Nephrology Flashcards
(291 cards)
1
Q
contrast nephropathy
What is contrast-induced nephropathy and what causes it⁉️
A
- ➡️ Contrast-induced nephropathy is a form of intrinsic acute kidney injury (AKI) caused by iodine-containing contrast used in CT scans.
💡 Most often transient and rarely requires dialysis.
2
Q
❓What are the two mechanisms of kidney injury in contrast-induced nephropathy (CIN)⁉️
A
1️⃣ Renal vasoconstriction ➡️ ⬇️ renal blood flow → pre-renal ischemia
2️⃣ Direct tubular toxicity ➡️ temporary tubular obstruction and damage (Renal )
🧠 NOTE: Together cause a mixed (pre-renal + intrinsic) acute kidney injury
3
Q
contrast nephropathy
Who is at increased risk of contrast-induced nephropathy⁉️
A
- 🚩 Patients with:
▪️ Chronic kidney disease (especially diabetic nephropathy)
▪️ eGFR < 30 mL/min/1.73 m²
▪️ Congestive heart failure (CHF)
▪️ Multiple myeloma
4
Q
contrast nephropathy
What is the typical timeline of serum creatinine changes after contrast exposure⁉️
A
➡️ Creatinine rises: 1–2 days after contrast
➡️ Peaks: on day 5
➡️ Resolves: by ~1 week
✅ Usually no irreversible damage
5
Q
contrast nephropathy
What is the best preventive strategy for contrast-induced nephropathy⁉️
A
✅ Hydration before contrast administration
BY IV 0.9% saline (1.0–1.5 mL/kg/hr)
▪️ 3–12 h before + 6–24 h after contrast
📉 Can reduce risk by >50%
📍 Also: Optimize volume status in heart failure
⛔ No proven benefit of bicarbonate or N-acetylcysteine]
6
Q
contrast nephropathy
Is oral hydration appropriate for preventing CIN in hospitalized patients⁉️
A
❌ No — IV fluids are preferred in hospitalized patients
✅ Oral hydration may be sufficient for low-risk, outpatient procedures
7
Q
contrast nephropathy
Why is furosemide not used for CIN prevention⁉️
A
⛔ Furosemide may worsen volume depletion
➡️ Does not ensure adequate hydration and may increase risk of CIN
8
Q
contrast nephropathy
What are the risk factors for contrast-induced nephropathy (CIN)⁉️
A
- Age > 80 years
- Chronic kidney disease (Cr > 2 mg/dL)
- Diabetic nephropathy
- Solitary kidney
- Dehydration
- Multiple myeloma / paraproteinemia
- Use of nephrotoxic drugs (e.g., NSAIDs, aminoglycosides)
- High contrast dose
- Congestive heart failure
9
Q
Allergic Interstitial Nephritis (AIN):
What are the typical features and timeline of drug-induced allergic interstitial nephritis (AIN)⁉️
A
- ➡️ Classic triad (rare):
▪️ Fever
▪️ Rash
▪️ Peripheral eosinophilia
🚩 Occurs 7–10 days after starting a drug (e.g. methicillin or other β-lactams)
10
Q
Allergic Interstitial Nephritis (AIN):
Which drugs are commonly associated with allergic interstitial nephritis (AIN)?
A
- 🚩 include:
▪️ β-lactam antibiotics (e.g. methicillin)
▪️ NSAIDs (nonsteroidal anti-inflammatory drugs)
▪️ Proton pump inhibitors (PPIs)
▪️ Anticonvulsants
▪️ Rare: sulfonamides, mesalazine/sulfasalazine, antiretrovirals
11
Q
allergic interstitial nephritis (AIN)
hat are the key urinalysis findings in allergic interstitial nephritis (AIN)⁉️
A
- Urinalysis shows:
▪️ Pyuria
▪️ White blood cell (WBC) casts
▪️ Hematuria - ⚠️ Urine eosinophils seen in 10–15% ➡️ Not sensitive or specific ⛔
12
Q
Allergic Interstitial Nephritis (AIN):
How useful are blood and urine eosinophils in the diagnosis of AIN ?
Allergic Interstitial Nephritis (AIN):
A
▪️ Peripheral eosinophilia: uncommon, but adds supportive evidence
▪️ Urinary eosinophils: more common but non-specific ⛔ Routine urine eosinophil testing not recommended
13
Q
Allergic Interstitial Nephritis (AIN):
Is a kidney biopsy required for diagnosis of allergic interstitial nephritis (AIN)⁉️
A
- ⚠️ Not usually required,
- but if done:
➡️ Shows interstitial & tubular leukocyte infiltration, including eosinophils
14
Q
Allergic Interstitial Nephritis (AIN):
What is the most important step in the management of allergic interstitial nephritis (AIN)⁉️
A
✅ Discontinuation of the offending drug
💡 Often leads to reversal of renal injury
15
Q
Acute kidney injury (AKI)
What are the diagnostic criteria for acute kidney injury (AKI)⁉️
A
📍 AKI is defined by:
▪️ Creatinine ↑ by ≥0.3 mg/dL or
▪️ Creatinine ↑ by ≥50% from baseline or
▪️ Urine output < 0.5 mL/kg/hr for ≥ 6 hours
16
Q
Acute kidney injury (AKI)
What are the main types of AKI and their causes⁉️
A
1.🚩 Pre-renal:
* Hypovolemia,
* ↓ Cardiac output (e.g. CHF)
* Liver failure
* NSAIDs, ACE inhibitors (↓ autoregulation)
2.🚩 Renal (intrinsic):
* ▪️ Glomerular
* ▪️ Tubular/interstitial (e.g. ischemia,sepsis , nephrotoxins)
* ▪️ Vascular (e.g. TTP/HUS, vasculitis)
3.🚩 Post-renal:
* Bladder outlet obstruction
* Bilateral pelvoureteral obstruction
17
Q
Acute kidney injury (AKI)
What is the most common cause of acute kidney injury (AKI)⁉️
A
🧠 Prerenal kidney injury is the most common etiology of AKI
18
Q
Acute kidney injury (AKI)
Which urinary casts finding are suggestive of prerenal kidney injury⁉️
A
Hyaline casts
19
Q
Acute kidney injury (AKI)
What are the key lab differences between pre-renal AKI and acute tubular necrosis (ATN)?? according to (BUN/Cr , Urine Na+ , FENa , Osmolality , Urine Sediment)
A
20
Q
Acute kidney injury (AKI)
How is treatment tailored based on AKI type⁉️
A
- 💧 Pre-renal:
▪️ Hypovolemia ➡️ Give fluids
▪️ Hypervolemia ➡️ Diuresis - 🧪 Post-renal:
▪️ US + Catheter + Nephrology consult - 💉 Renal:
▪️ Remove offending agent, treat underlying cause
21
Q
Acute kidney injury (AKI)
When is dialysis indicated in AKI⁉️
A
- ✅ Use the mnemonic U-E-A-I-O (vowels):
🔹 Uremia ➡️ pericarditis, encephalopathy, bleeding
🔹 Electrolyte imbalance ➡️ refractory hyperkalemia
🔹 Acidosis ➡️ unresponsive metabolic acidosis
🔹 Intoxication ➡️ drug/toxin ingestion
🔹 Overload ➡️ volume overload unresponsive to diuretics (e.g. pulmonary edema)
22
Q
Acute kidney injury (AKI)
What are the main nephrotoxins causing intrinsic AKI⁉️
A
🔻 Endogenous: Hemolysis, rhabdomyolysis, myeloma, crystals
🔻 Exogenous: Iodine contrast, aminoglycosides, cisplatin, amphotericin B, PPIs, NSAIDs
23
Q
Acute kidney injury (AKI)
What lab findings are suggestive of pre-renal acute kidney injury (AKI)⁉️
A
🧪 Key findings:
* 🔹 High BUN-to-creatinine ratio ➡️ >20:1
* 🔹 FENa < 1%
* 🔹Urine osmolality >500
* 🔹 Concentrated urine ➡️ Specific gravity >1.020
🔹Hyaline casts ✅
* 🔹 Normal urinalysis ➡️ Few leukocytes, no casts
fractional excretion of sodium (FENa) measures filtered sodium in urine
24
Q
Acute kidney injury (AKI)
Why is BUN:Creatinine ratio elevated in pre-renal injury⁉️
A
➡️ Decreased renal perfusion ➡️ kidney reabsorbs more urea
✅ Urea increases more than creatinine
📈 Leads to BUN:Cr >20:1
25
# Acute kidney injury (AKI)
How does the **fractional excretion of sodium (FENa**) help identify **pre-renal AKI**⁉️
✅ **FENa < 1%** means **sodium is being avidly reabsorbed**
**Sign of intact tubular function trying to conserve volume**
26
# Acute kidney injury (AKI)
What does **high urine specific gravity** indicate in **pre-renal injury⁉️**
📍 Urine specific gravity >1.020
➡️ **Kidneys concentrate urine** to conserve water
✅ **Suggests functional tubules**
27
# Acute kidney injury (AKI)
What is the most likely **cause** of **pre-renal azotemia** in a patient **on diuretics** with **hypovolemia**⁉️
🚩 **Volume depletion** due to **diuretics**
➡️ Leads to **reduced renal perfusion** and **classic pre-renal lab pattern**
28
# Acute kidney injury (AKI)
What are the **major causes** of a**cute tubular necrosis (ATN)⁉️**
📍 Two main categories:
* 🔻**Ischemia**
▪️ Prolonged **hypotension**
▪️ **Sepsis**
▪️ **Cardiogenic shock**
* 🔻**Nephrotoxins**
1. **Endogenous**:
▪️ Hemolysis
▪️ Rhabdomyolysis
▪️ Myeloma
▪️ Intratubular crystals
2. **Exogenous**:
▪️ Iodine contrast
▪️ Aminoglycosides
▪️ Cisplatin
▪️ Amphotericin B
▪️ NSAIDs
▪️ PPIs
29
# Acute kidney injury (AKI)
What are the **classic lab** and **urine findings** in **acute tubular necrosis (ATN**)⁉️
▪️ **Muddy brown granular casts**
▪️ **FeNa > 2%**
▪️ **BUN/Creatinine ratio ~10-15**
▪️ **Urine Na⁺: >40 m**Eq/L
▪️ **Urine osmolality: < 350 mOs m/kg**
* 🧠 **Indicates** **intrinsic renal injury (tubular)**
30
# Acute kidney injury (AKI)
What **BUN:Cr ratio** is indicative of **pre-renal azotemia⁉️**
✅ **BUN:Cr > 20**
💡 Indicates increased urea reabsorption due to decreased renal perfusion
31
# Acute kidney injury (AKI)
What is the **typical course of acute tubular necrosis** (ATN) if the **underlying cause is corrected**⁉️
🕒 **May** **resolve within ~2 weeks after restoration of renal perfusion**
✅ **Supportive care** and **correction** of ischemia/toxin exposure often lead to recovery
32
# Acute kidney injury (AKI)
What is the most likely cause of **AKI** in a patient with **immobilization and drug intoxication**⁉️
* 🚩 **Rhabdomyolysis-induced AKI**
* mechanism:
**Immobilization** → **muscle breakdown** → **myoglobin release** ➡️ Direct **tubular toxicity** & **obstruction**
* **Leads to acute tubular necrosis (ATN) → renal (intrinsic) AKI**
33
# Acute kidney injury (AKI)
What **endogenous nephrotoxins** can lead to **ATN**?
* 🔻 Endogenous causes of ATN:
▪️ **Hemolysis**
▪️ **Rhabdomyolysis**
▪️ **Myeloma**
▪️ **Intratubular crystals**
34
# Acute kidney injury (AKI)
What is **the most specific** lab test to confirm rhabdomyolysis⁉️
✅ **Elevated serum creatine phosphokinase** (CPK)
35
# Acute kidney injury (AKI)
What are the key **lab findings** in **rhabdomyolysis-associated AKI**⁉️
🧪 Labs show:
▪️ **↑ Creatinine**
▪️ **↑ Creatine kinase (CK)**
▪️ **↑ AST** (from **muscle**, not liver)
▪️ Positive **urine myoglobin**
📍 **Oliguria** & **dark-colored urine** are common
36
# Acute kidney injury (AKI)
What is the **most feared complication** of rhabdomyolysis⁉️
🚨 **Acute kidney injury (AKI)**
✅ Caused by myoglobin-induced tubular damage
➡️ Myoglobin is nephrotoxic and leads to acute tubular necrosis
37
# Acute kidney injury (AKI)
What should be suspected when urinalysis is **positive for blood but no RBCs** are seen on microscopy⁉️
🧠 **Rhabdomyolysis**
* 🔬 Confirm with **elevated Creatine Phosphokinase** (CPK) levels
* 💡 **Myoglobin in urine causes false-positive dipstick for blood**
* ⛔ **No RBCs seen under microscope**
38
# Acute kidney injury (AKI)
How is **AKI due to rhabdomyolysis** **managed**⁉️
💧 **Aggressive IV fluids**
🧪 Correction of **electrolyte abnormalities**
* ⚠️ **Goal**: **prevent myoglobin-induced tubular injury**
39
# Acute kidney injury (AKI)
What are the major **causes of rhabdomyolysis**⁉️
✅ **Crush injuries** / **trauma**
✅ **Convulsions** / seizures
✅ **Infections**
✅ **Medications**:
* Statins + fibrates
✅ **Strenuous exercise**
✅ **Inflammatory myopathies**
✅ **Electrolyte imbalances**:
* Hypokalemia
* Hypophosphatemia
✅ **Severe hypothyroidism**
✅ **Neuroleptic malignant syndrome (NMS**)
40
Why is aggressive **IV saline preferred** over **mannitol**, **diuretics**, or **NAC** (N-acetylcysteine) in rhabdomyolysis⁉️
✅ **0.9% NaCl is the first-line treatment**
🧠 It **restores volume**, **maintains perfusion**, and **flushes out myoglobin**
41
# Acute kidney injury (AKI)
What is the **most lethal complication** of rhabdomyolysis⁉️
🚨 **Acute kidney injury (AKI)**
🧠 Due to **myoglobin-induced tubular toxicity**
42
# Acute kidney injury (AKI)
❓What are the **electrolyte abnormalities** seen in rhabdomyolysis⁉️
⬆️**K⁺**
⬆️**Phosphate**
⬇️ **Calcium**
💡**Due to massive tissue breakdown**
43
# Acute kidney injury (AKI)
Why is **AST elevated in rhabdomyolysis**, and how can it be **distinguished from liver injury**⁉️
➡️ **AST is released from damaged muscle cells**
⛔ **Not from liver** (e.g. not paracetamol-induced hepatotoxicity)
* **Confirm with high CK and urinary myoglobin**
44
# Acute kidney injury (AKI)
What is the **first step** when **urinary tract obstruction is suspected**⁉️
🛑 **Insert a bladder catheter** to:
➡️ Relieves obstruction
➡️ Prevents **renal damage and urinary tract infection**
45
# SIADH
What is Syndrome of Inappropriate Antidiuretic Hormone secretion (**SIADH**)⁉️
* SIADH is a condition characterized by:
➡️ **Excessive ADH secretion despite normal or low plasma osmolality**
* ADH acts on the kidneys:
➡️ Binds to V2 receptors in the collecting ducts
➡️ **Promotes free water reabsorption** ➡️ **concentrated urine**
* 💧 This leads to:
▪️ **Water retention**
▪️ **Dilutional hyponatremia**
▪️ **Euvolemic status (no edema or hypovolemia)**
📍 ***Serum***: **hyponatremia + low osmolality**
📍 ***Urine***: **inappropriately concentrated + high sodium**
46
# SIADH
What is the **normal action of antidiuretic hormone (ADH) in the body**⁉️
* **ADH (vasopressin**) is secreted by the posterior pituitary
* **in** **response to**:
▪️ Increased plasma osmolality
▪️ Hypovolemia or hypotension
* 💧 **ADH acts on the kidneys:**
➡️ Binds to V2 receptors in the collecting ducts
➡️ **Promotes free water reabsorption** ➡️ **concentrated urine**
47
# SIADH
What are the **major causes** of SIADH⁉️
* **Etiologies**:
▪️ **Pulmonary**: Pneumonia, lung abscess, pleural effusion
▪️ **CNS**: SAH, meningitis, tumors
▪️ **Malignancies**: Small cell lung cancer, brain tumors
▪️ **Drugs**: SSRIs, TCAs, antiepileptics
▪️ **Severe pain or nausea**
48
# SIADH
What is **the most common cause** of **euvolemic hyponatremia** ??
* ✅ **Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)**
📍 Others:
▪️ Hypothyroidism
▪️ Secondary Addison’s disease
▪️ Primary polydipsia (psychogenic)
49
# SIADH
What **lab findings** support the diagnosis of SIADH⁉️
SIADH:
▪️ **High urine osmolality >400 mOsm/kg**
▪️ **Urine Na⁺ >20–30 mEq/L**
📍 **Inappropriate concentration despite hyponatremia**
50
# SIADH
w do you differentiate **SIADH from primary polydipsia** using **labs**⁉️
SIADH ➡️ **Urine osmolality >400**
▪️ Primary polydipsia ➡️ **Urine osmolality < 100**
▪️ Osmolality 100–400 ➡️ Mixed or transitional disorder
51
# SIADH
How can you distinguish **SIADH** from **hypovolemic hyponatremia** when **values are borderline**⁉️
💡 Give **normal saline and observe response**:
* ▪️ **SIADH** ➡️ **Na⁺ does not correct** or worsens
▪️ **Hypovolemia** ➡️ **Na⁺ improves**
52
# SIADH
What is the **first-line** treatment for SIADH⁉️
✅ **Fluid restriction**
📍 **Alternatives if ineffective or intolerable**:
▪️ **Saline infusion**
▪️ **Salt tablets**
▪️ **Loop diuretics (e.g. furosemide**)
53
# SIADH
Why is **Addison’s disease unlikely** in a patient with **isolated hyponatremia**⁉️
⛔ Addison’s disease causes:
▪️ **Hyponatremia** **PLUS**
▪️ **Hyperkalemia**
▪️ **Hypoglycemia**
🧠Not supported if these are absent
54
# SIADH
What **symptoms** may occur in **SIADH** and hyponatremia⁉️
📍 **Depends** on **rate/severity** of **Na+ drop**:
▪️ **Mild**: Nausea, headache, vomiting
▪️ **Severe**: Seizures, coma
55
# SIADH
How is **hyponatremia treated** based on **severity**⁉️
▪️ **Severe symptomatic** (seizures, coma) ➡️( **3% hypertonic saline**)
▪️ **Hypovolemic** hyponatremia ➡️ **0.9% isotonic saline**
56
# SIADH
Why must **sodium correction** in hyponatremia be done **cautiously**?
🚨 Rapid correction of sodium can cause:
➡️ **Osmotic Demyelination Syndrome** (ODS): Severe, **irreversible damage to central pontine myelin**
⚠️ Note: **Do not exceed Na⁺ rise of 8–10 mEq/L in 24 hours**
57
# SIADH
**What are the 3 volemic states in hypotonic hyponatremia and causes**
58
What diagnosis is suggested by **confusion**, **severe hypernatremia (Na⁺ 165**), **polyuria**, and **dilute urine (urine osmolality 100 mOsm/kg)⁉️**
✅ **Nephrogenic diabetes insipidus (NDI)**
🧠 Caused by **renal resistance to ADH** ➡️ **inability to concentrate urine**
📍 Common cause: **Chronic lithium use**
59
What medication commonly causes **nephrogenic diabetes insipidus** (NDI)⁉️
💊 **Chronic lithium therapy**
🧠 Lithium damages **collecting duct cells**, impairing **response to antidiuretic hormone (ADH**)
60
How does **lithium** cause **nephrogenic diabetes insipidus (NDI)⁉️**
🧠 Lithium **damages collecting duct cells**, interfering with **ADH action**
📉 Result:
▪️ Impaired water reabsorption
▪️ Polyuria
▪️ Dilute urine
➡️ **Leads to dehydration and hypernatremia**
61
# focal segmental glomerulosclerosis (FSGS)
What is **focal segmental glomerulosclerosis** (FSGS), and what are its **causes**⁉️
🧠 FSGS is a **nephrotic syndrome** marked by **segmental** scarring of **some** glomeruli
📍 Can be:
* ▪️ **Primary** (**idiopathic**) MOST COMMON
* ▪️ **Secondary**
62
# focal segmental glomerulosclerosis (FSGS)
What are the **clinical features of FSGS**⁉️
📍 Classic **nephrotic** features:
▪️ **Proteinuria** (often nephrotic range)
▪️ **Hematuria**
▪️ **Hypertension**
▪️ Progressive **renal insufficiency**
63
# focal segmental glomerulosclerosis (FSGS)
What is the **prognosis** and **recurrence** of FSGS **after transplant**⁉️
* 📉 **50% progress to renal failure within 8 years**
* 🔁 **40% recurrence in renal transplant recipients**
64
What are the hallmark features of **nephrotic syndrome⁉️**
▪️ **Proteinuria** >3 g/24h
▪️ **Hypoalbuminemia**
▪️ **Edema** / Anasarca
▪️ **Hypercholesterolemia**
▪️ ± **Microscopic hematuria**
▪️ ± **Hypertension**
65
# membranous glomerulonephritis (MGN)
What are the **causes of membranous glomerulonephritis (MGN)⁉️**
* 📍 **Primary** **(idiopathic)** ➡️ majority of cases
* 📍 **Secondary** (20–40%) to:
▪️ **Solid tumors**: breast, lung, colon
▪️ **Infections**: HBV, malaria, schistosomiasis
▪️ **Autoimmune**: SLE, rheumatoid arthritis
▪️ **Medications** (e.g., NSAIDs)
66
What are the major **complications** of nephrotic syndrome⁉️
🚨 Complications include:
✅ **Infections** ➡️ due to hypogammaglobulinemia
✅ **Thrombosis** ➡️ especially **renal vein thrombosis** when albumin < 2 g/dL
✅ **Hypertension**
nephrotic syndrome next?
67
What **distinguishes** **idiopathic** MGN (IMN) from **secondary** MGN⁉️
🧬 **IMN**: **Anti-PLA2R antibodies** found in ~**70**%
⛔ Usually **absent** in secondary MGN
68
What is **the most common cause of nephrotic syndrome** in adults **aged 30–50⁉️**
* ✅ **Membranous nephropathy**
📊 Accounts for ~20% of adult nephrotic syndrome cases
📍 More common in males (2:1)
69
# membranous glomerulonephritis (MGN
What **complication** is commonly associated with membranous glomerulonephritis⁉️
⚠️ **Venous thromboembolism** (e.g. renal vein thrombosis)
🧠 Especially when serum albumin < 2 g/dL
70
hat **causes the increased risk of venous thromboembolism** in membranous glomerulonephritis⁉️
🚨 **Loss of anticoagulant proteins** (e.g., antithrombin III) in urine
➡️ Leads to **hypercoagulability and RVT**
71
How is renal vein thrombosis **diagnosed** in patients with nephrotic syndrome⁉️
🔬 **Renal vein Doppler ultrasound**
✅ Non-invasive and effective diagnostic tool
72
# membranous glomerulonephritis (MGN
Why should **malignancy screening** be performed in patients with **membranous nephropathy**⁉️
* 🧠 **20–30% of membranous nephropathy cases are secondary**
* 🔍 **Malignancies (breast, colon, lung, etc.) are common secondary causes**
* 📌 Perform **age-appropriate cancer screening** **based on risk factors**
73
# membranous glomerulonephritis (MGN
What are the **clinical signs** of **renal vein thrombosis in nephrotic syndrome⁉️**
* 🚨 May be **asymptomatic** or present with:
▪️ **Flank pain & tenderness**
▪️ **Hematuria & proteinuria**
▪️ **Sudden drop in renal function**
🧠 More common in the **left renal vein**
🔁 **2/3 of cases are bilateral**
74
What **type** of glomerular syndrome does **membranous glomerulonephritis** (MGN) cause⁉️
🧪 **Nephrotic syndrome**
✅ Characterized by **subepithelial immune deposits**
✅ Accounts for ~**25% of adult nephrotic syndrome cases**
75
# membranous glomerulonephritis (MGN)
What are the **characteristic findings** of MGN on **renal biopsy**⁉️
✅ **Light microscopy**: Thickened glomerular basement membrane
✅ **Immunofluorescence**: Granular IgG + C3 deposition
✅ **Electron microscopy**: **Subepithelial immune deposits**
76
# membranous glomerulonephritis (MGN)
What is the **prognosis** of membranous glomerulonephritis (MGN)⁉️
📊 Prognosis distribution:
1️⃣ **⅓** → **Spontaneous** **remission**
2️⃣ **⅓** → **Relapsing nephrotic syndrome** (normal renal function)
3️⃣ **⅓** → Progression to **renal failure**
77
# membranous glomerulonephritis (MGN)
What are **complications** of membranous glomerulonephritis (MGN)⁉️
🚨 **Thromboembolic risk:**
✅ Renal vein thrombosis
✅ Other thrombophilic disorders (due to urinary loss of anticoagulants)
78
# membranous glomerulonephritis (MGN
Why are patients with **nephrotic syndrome**, especially **membranous glomerulonephritis** (MGN), **at risk for renal vein thrombosis⁉️**
🧠 **Loss of anticoagulant proteins** (e.g. antithrombin III, protein C/S) in urine
📉 **Risk increases when albumin < 2 g/dL**
⚠️ Leads to **hypercoagulable state** ➡️ **venous thromboembolism**
✅ Common site: renal vein thrombosis
79
What is the **first-line treatment** approach in **idiopathic MGN (IMN) with nephrotic syndrome⁉️**
▪️ **ACE inhibitors or ARBs** → Control proteinuria & BP
▪️ **Statins** → Manage dyslipidemia
▪️ **Diuretics** → Relieve edema
80
When is **immunosuppressive** therapy indicated in **idiopathic membranous nephropathy (IMN)⁉️**
🚨 **If persistent proteinuria despite supportive therapy**
➡️ Use:
▪️ **Steroids** + **cyclophosphamide**
▪️ Or **MMF**, **chlorambucil**, **cyclosporine**, **rituximab**
81
# focal segmental glomerulosclerosis (FSGS),
What are the **clinical features of FSGS**⁉️
| focal segmental glomerulosclerosis (FSGS),
📍 Classic nephrotic syndrome signs:
▪️ **Proteinuria** (nephrotic range)
▪️ **Hematuria**
▪️ **Hypertension**
▪️ **Renal insufficiency**
82
# focal segmental glomerulosclerosis (FSGS),
What is the **prognosis** and **recurrence rate** of **FSGS** after **kidney transplant**⁉️
| focal segmental glomerulosclerosis (FSGS),
📉 **50% develop renal failure within 8 years**
🔁 Up to **40% may have recurrence in transplanted kidneys**
83
# focal segmental glomerulosclerosis (FSGS),
How does FSGS respond to **steroid** therapy⁉️
| focal segmental glomerulosclerosis(FSGS),
⛔ **Poor** response to steroids
🧠 Often **resistant nephrotic syndrome**
84
What defines a **hypertensive emergency** and what is its **renal manifestation**⁉️
* 🚨 Hypertensive emergency =
▪️ **BP ≥180/120 mmHg with signs of target-organ damage,** such as:
▪️ CNS: Encephalopathy (HA, confusion, nausea)
▪️ Cardiac: Acute heart failure, ACS
▪️ Vascular: Aortic dissection
▪️ Renal: AKI, hematuria, RBC casts
* 🧪 **Renal target-organ damage:**
▪️ Acute kidney injury
▪️ Hematuria
▪️ Red blood cell casts on urine sediment ✅
85
What are the **signs** of **target-organ damage** in hypertensive emergency⁉️
🧠 **CNS**: **Headache**, confusion, nausea**/vomiting** ➡️ hypertensive **encephalopathy**
💔 **Heart**: Acute **heart failure**, pulmonary edema, acute coronary syndrome
🔪 **Vessels**: Acute **aortic dissection**
🧪 **Kidneys**: AKI with **RBC casts** on urinalysis
86
What is the typical **urine sediment finding** in hypertensive emergency⁉️
🔬 **Red blood cell casts**
🧠 Indicates **glomerular injury due to severe hypertension**
87
What makes **metabolic acidosis** an **urgent indication for dialysis**⁉️
📉 **Severe**, **refractory acidosis** (e.g., pH < 7.2, HCO₃⁻ < 15 mEq/L)
88
hat is the **GFR threshold for considering dialysis⁉️**
* 📉 Dialysis is typically **initiated** when:
➡️ **GFR < 10 mL/min/1.73 m²**
89
**Hyaline casts** , what do they indicate ?
🧪 Seen in **pre-renal AKI** (low perfusion states)
90
What clinical and **imaging feature suggests chronic kidney disease** (CKD) rather than acute kidney injury (AKI)⁉️
🔬 **Ultrasound finding:**
✅ **Small**, **hyperechoic kidneys** with **thin cortex** ➡️ **suggest CKD**
🧠 Note: **Radiographic bone disease** also **supports CKD** but appears **late**, especially in dialysis patients
91
**Muddy Brown Granular Casts**
What is the diagnosis?
**Acute Tubular Necrosis (ATN)**
**Most specific cast for ATN**
92
**White Blood Cell (WBC) Casts**
Which conditions are linked?
**Acute Interstitial Nephritis** (AIN)
or
**Pyelonephritis**
**Inflammation or infection of tubules/interstitium**
May present with fever, rash (AIN), or flank pain (pyelo)
93
**Fatty Casts** ("**Maltese cross**" under polarized light)
What do they indicate?
* **Nephrotic Syndrome**
Sign of **heavy proteinuria and lipiduria**
94
What are **classic features** of chronic kidney disease (CKD)⁉️
📉 **Decreased GFR, increased creatinine**
🧠 Key findings:
▪️ **Small, shrunken kidneys on ultrasound**
▪️ **Secondary hyperparathyroidism** → 🦴 Renal osteodystrophy
▪️ **Anemia** (due to ↓ erythropoietin)
📍 **Electrolyte abnormalities**:
▪️ **Hyperphosphatemia**
▪️ **Hypocalcemia**
▪️ **Hyperkalemia** (also seen in AKI)
95
# chronic kidney disease (CKD)
What type of **anemia** is commonly associated with chronic kidney disease (CKD), and from **which stage** does it typically appear?
✔️ **Normocytic, normochromic anemia**
✔️ Typically **appears from CKD stage 3**
✔️ Present in almost all patients by stage 4
96
Why is **proteinuria** **not** a reliable feature to differentiate AKI from CKD⁉️
⛔ Because proteinuria can **occur in both AKI and CKD**
97
What is the significance of a **monoclonal spike in blood** in renal failure⁉️
Indicates possible **multiple myeloma**
* ⚠️ Can cause both CKD and AKI-on-CKD (e.g., via hypercalcemia, drugs, tubular injury)
98
What are the typical **iron studies** in **CKD-related anemia**⁉️
* Normal **Serum iron**
* Normal **TIBC** (total iron-binding capacity)
* Normal **Ferritin**
* 📌 **Helps distinguish CKD from iron-deficiency anemia**
99
# chronic kidney disease (CKD)
Why is **parathyroid hormone (PTH) elevated** in **chronic kidney disease (CKD)⁉️**
🧠 CKD causes:
▪️ ↓ phosphate excretion → **hyperphosphatemia**
▪️ ↓ vitamin D activation → **↓ calcium absorption**
📉 Result: **hypocalcemia**
➡️ **Stimulates ↑ PTH release** → **secondary hyperparathyroidism**
100
What are the **hallmark features of chronic kidney disease** (CKD)⁉️
🧠 Key features of CKD:
✅ **Decreased GFR**
✅ **Increased creatinine**
✅ **Small kidneys** on **ultrasound**
✅ **Secondary hyperparathyroidism** ➡️ renal osteodystrophy
✅ **Anemia (normocytic**) — but can also appear in AKI
101
Why are **proteinuria, hyperkalemia, anemia, and elevated creatinine** **not exclusive** to CKD⁉️
⛔ Because **these findings can also be present in acute kidney injury** (AKI) or **even without kidney failure** (e.g., isolated proteinuria)
102
# chronic kidney disease (CKD)
Why are **erythropoietic stimulating agents**(ESAs) **preferred over blood transfusions** in CKD-associated anemia today?
✔️ **Avoids transfusion-related complications** such as:
- 🦠 **Infections**
- ⚠️ **Iron overload**
- 🧬 **Alloantibody development**
✔️ **Targets a safer hemoglobin range (10–11.5 g/dL)**
✔️ Stimulates **natural erythropoiesis**
103
# chronic kidney disease (CKD)
How does CKD affect **phosphate** levels⁉️
📈 **Increased phosphate** (hyperphosphatemia)
🧠 Due to **reduced renal excretion of phosphate**
104
# chronic kidney disease (CKD)
What fluid and **electrolyte disturbances** are commonly seen in **CKD**⁉️
📉 **Hyponatremia**,
📈 **Hyperkalemia**, **Hyperphosphatemia**,
🧪 **Metabolic acidosis**
105
# chronic kidney disease (CKD)
In which CKD-related condition is **fluid restriction** recommended⁉️
**Chronic kidney disease and hyponatremia**
🧠 Especially in the setting of **hypervolemia** (fluid overload)
📌 **Sodium and water restriction helps correct dilutional hyponatremia**
106
# chronic kidney disease (CKD)
How does CKD affect **calcium** levels⁉️
📉 **Decreased calcium** (hypocalcemia)
🧠 Caused by:
▪️ Phosphate retention (**binds calcium**)
▪️ **↓ Calcitriol** (vitamin D activation) → **↓ GI calcium absorption**
107
# chronic kidney disease (CKD)
Why do **CKD patients develop anemia**⁉️
🧠 Due to **↓ erythropoietin (EPO) production** by the damaged kidneys
📉 Anemia typically **starts** in **CKD stage 3,** and is almost **universal by stage 4**
108
# chronic kidney disease (CKD)
How is **anemia** in CKD **treated**⁉️
💉 **Erythropoietin (EPO) therapy** is the main treatment
🎯 **Goal** Hb: **10–11.5 g/dL**
109
# chronic kidney disease (CKD)
What **lab values must be assessed** **before starting ESA** therapy in CKD patients, **and why**?
* ✔️ **Ferritin** – to assess iron stores
* ✔️ **Transferrin saturation (TSAT)** – to evaluate iron availability
* 📌 **Ensures the bone marrow is responsive to ESA therapy**
110
# chronic kidney disease (CKD)
What additional **treatments are usually given alongside ESA** therapy in CKD-related anemia, and **what is their purpose?**
✔️ **Iron supplements** – support red cell production
✔️ **Vitamin B12** – essential for DNA synthesis in RBCs
✔️ **Folate (folic acid)** – aids in erythropoiesis
* 🧠 **These address potential coexisting deficiencies that impair response to ESA**
111
# chronic kidney disease (CKD)
Compare **past and current treatments for anemia in CKD**.
What are the key differences?
112
# chronic kidney disease (CKD)
What is the **primary cause** of **normocytic, normochromic** anemia in patients with **chronic kidney disease** (CKD) stage IV–V?
**Erythropoietin (EPO) deficiency** 🧬
- EPO is produced by the kidneys, and its deficiency leads to reduced red blood cell production in CKD.
- This results in normocytic, normochromic anemia — normal size and color but fewer RBCs.
113
# chronic kidney disease (CKD)
What are the **two main types** of normocytic anemia **based on reticulocyte index (RPI)⁉️**
🔻 **Hypoproliferative** (RPI < 2)
1. Bone marrow failure
2. Aplastic anemia
3. Renal disease (e.g. CKD)
4. Myelofibrosis
5. Leukemia
🔺 **Hemolysis or hemorrhage** (RPI > 2)
114
# chronic kidney disease (CKD)
When should **erythropoietin therapy** be started in CKD⁉️
* 💉 Start EPO therapy if:
▪️ **Hemoglobin < 10 g/dL**
* ▪️ Treatment is started **only after ensuring Iron stores are adequate** BY check ferritin & transferrin saturation (TSAT)
* 📍NOTE: **Always correct iron deficiency before or alongside EPO**
115
What is **the most common cause** of **death** in patients with chronic kidney disease (CKD)⁉️
🚨 **Cardiovascular disease (CVD**)
116
What **percentage of CKD stage 5** patients have **cardiovascular complications**⁉️
📊 Up to **45%** of stage 5 CKD patients
117
How does **chronic kidney disease** (CKD) affect **troponin levels⁉️**
* 🧪 CKD patients often have **chronically elevated troponin without acute ischemia**
* ⚠️ Persistent elevation = poor prognosis
118
What **cardiovascular risk factors** are commonly associated with CKD⁉️
🚩 **Hypertension**
🚩 **Left ventricular hypertrophy**
🚩 **Dilated cardiomyopathy**
🚩 **Diabetes mellitus**
🚩 **Ischemic heart disease (IHD**)
🚩 **Congestive heart failure (CHF)**
119
What are the **recommendations** for **managing cardiovascular risk in CKD patients⁉️**
* 🩺 **Close monitoring** + **Pharmacological therapy**
* ➡️ **Target BP**, **glucose**, and **lipid control**
* ✅ **Prevent progression of both CKD and CVD**
120
# chronic kidney disease (CKD)
❓What is the **best next step** after **confirming persistent hematuria**⁉️
* **Collect urine sample** to check for:
▪️ **Casts** (e.g., RBC casts → glomerular origin)
▪️ **24-hour urine protein**
📍 If **proteinuria >500** mg/day ➡️ **further evaluation for glomerulonephritis is indicated**
121
# chronic kidney disease (CKD)
What conditions must be considered in the **differential diagnosis of hematuria⁉️**
🧠 Causes include:
▪️ **Glomerulonephritis**
▪️ **Nephrolithiasis**
▪️ **Tumors** (e.g., RCC, bladder cancer)
▪️ **Trauma**
122
# chronic kidney disease
What is **the most common cause of chronic kidney** disease (CKD) in North America and Europe⁉️
**Diabetic nephropathy**
📍 Especially due to **type 2 diabetes mellitus**
📈 **Leading cause of end-stage renal disease (ESRD) in developed countries**
123
# chronic kidney disease
hat is the **target hemoglobin** level for treating anemia in **CKD patients**⁉️
🎯 **10–11.5 g/dL**
🧠 Higher levels may increase cardiovascular risk
➡️ **Avoid overcorrection**
124
# chronic kidney disease
What are **the common causes** of chronic kidney disease (CKD
1️⃣ **Diabetic nephropathy ✅ (most common)**
2️⃣ **Glomerulonephritis**
3️⃣ **Hypertension**
4️⃣ **Autosomal Dominant Polycystic Kidney Disease (ADPKD)**
5️⃣ **Tubulointerstitial nephropathy**
125
# chronic kidney disease
How does **kidney size** vary in different causes of **chronic kidney disease⁉️**
1. 🧪 **Small kidneys** ⬇️
▪️ **Hypertension** ➡️ tubular ischemia → fibrosis → atrophy
2. 🧪 **Normal to enlarged kidneys ⬆️**
▪️ **Diabetes mellitus**
▪️ **HIV nephropathy**
▪️ **Amyloidosis**
126
# chronic kidney disease
Why are **kidneys enlarged** in **diabetic nephropathy⁉️**
**Glomerular basement membrane thickening**
📈 Leads to **hyperfiltration**, ↑ **intraglomerular pressure**, and **glomerular hypertrophy**
➡️ Renal size increases
127
What renal **imaging finding** is characteristic of **amyloidosis** in **chronic kidney disease**⁉️
🔍 **Bilaterally enlarged kidneys**
🧠 Seen in amyloidosis due to **extracellular deposition** of insoluble amyloid proteins
128
What are the **main types of amyloidosis** and their associated diseases⁉️
📌 Types of amyloid and associations:
✅ **AL** (**light chains**): Multiple myeloma, lymphoma
✅ **AA** (**serum amyloid A**): Chronic inflammatory diseases (RA, FMF, IBD)
✅ **ATTR** (**transthyretin**): Familial amyloidosis
✅ **Aβ** (**beta-amyloid**): Alzheimer’s disease
129
How is amyloidosis **diagnosed histologically**⁉️
:
🔬 Diagnosis via **fat pad biopsy**
✅ Staining with **Congo red** → apple-green birefringence under polarized light
✅ Followed by **immunohistochemistry** to identify amyloid type
130
Which **organ** is most frequently affected in **amyloidosis**, and what are other common manifestations⁉️
🧠 Most affected organ: **Kidneys** **(70–80%)**
Other findings:
✅ Hepatosplenomegaly
✅ Autonomic neuropathy
✅ Restrictive cardiomyopathy
131
What is the **treatment approach** for renal amyloidosis⁉️
💊 Focus is on **treating the underlying cause**
➡️ Reduces **serum amyloid A** or **light chains** depending on the type
132
# chronic kidney disease
Why does **amyloidosis** cause **enlarged** kidneys⁉️
📍 **Amyloid** **infiltration** of **glomeruli** and **tubules**
➡️ Causes **kidney enlargement** due to **protein deposition**
133
# chronic kidney disease
Why do kidneys become **small** in chronic kidney disease due to **hypertension**⁉️
**Hypertension** → **narrowing of afferent arterioles**
⬇️ Leads to **↓ glomerular blood flow** → **tubular ischemia**
➡️ Progressive **sclerosis**, **fibrosis**, and **atrophy**
📉 Result: **Small, shrunken kidneys**
134
# IgA nephropathy
What **classic presentation** suggests IgA nephropathy (**Berger’s disease**)⁉️
* 🧒🏼 **Recurrent episodes** of **gross (macro) hematuria**
* 💡 Occurring **within days of an upper respiratory tract infection (URTI)**
* 📍 May also present as **persistent asymptomatic microscopic hematuria**
135
# IgA nephropathy
What **findings** in a **urinalysis** strongly indicate **glomerular disease as the cause of hematuria**?
✔️ **Macrohematuria** or **microscopic hematuria**
✔️ Presence of **dysmorphic red blood cells** 🧬
✔️ **RBC casts**
✔️ **Proteinuria >500** mg/day 💧
📌 All these point toward glomerulonephritis as the underlying pathol
136
# IgA nephropathy
How is IgA nephropathy **diagnosed**⁉️
* 🔬 **Renal biopsy** : Confirms mesangial IgA deposition
137
# IgA nephropathy
What does the presence of **isolated hematuria without proteinuria** **or casts** suggest?
* ✔️ **Non-glomerular source of bleeding**
🔹 Examples: Urinary tract stones, tumors, trauma
✔️ Not usually associated with dysmorphic RBCs or proteinuria
138
# IgA nephropathy
How does **hematuria caused by urinary tract infections** typically present?
✔️ **Hematuria** + **pyuria** (WBCs in urine) 🔥
✔️ Often **associated with dysuria, urgency, and frequency**
📌 Suggests **lower urinary tract origin**, **not glomerular**
139
# IgA nephropathy
Compare **glomerular vs. non-glomerular hematuria**: key urine findings and likely causes ?
140
# IgA nephropathy
What is the **typical prognosis** for patients with IgA nephropathy?
✔️ **Good prognosis overall**
✔️ **25-30% of patients may progress to renal failure over 20-25 years** ⏳
📌 **Majority** of patients have **stable kidney function long-term**
141
What is the **treatment approach** for IgA nephropathy **based on clinical severity**⁉️
💊 Treatment **depends on severity**:
✅ **ACE inhibitors** – for **hypertension + proteinuria**
✅ **Steroids, cytotoxic agents, plasmapheresis** – for **RPGN**
✅ **No immunosuppressive therapy** – for **asymptomatic patients with minimal proteinuria and normal function** ➡️ **monitor only**
142
# IgA nephropathy
Which **demographic** is most commonly affected by IgA nephropathy?
* ✔️ **Men**, **aged 2–3 decades** 🧑⚕️
* ✔️ Usually **sporadic in nature (not inherited)**
143
# IgA nephropathy
What is the **pathologic hallmark** of IgA nephropathy⁉️
**IgA deposition in the mesangium** , Confirmed via renal **biopsy with immunofluorescence**
144
# IgA nephropathy
Is serum **IgA level diagnostic** for IgA nephropathy⁉️
* **No** – Serum IgA may be elevated in 20–50% of cases
🧪 It is not specific or sufficient for diagnosis
* ✅ **Renal biopsy is mandatory to confirm mesangial IgA depositio**
145
What are **poor prognostic factors** in IgA nephropathy⁉️
🚩 Associated with faster progression to CKD:
▪️ **Hypertension**
▪️ **Persistent proteinuria** (>6 months)
▪️ **Absence of episodic macrohematuria**
▪️ **Male sex**
▪️ **Older age**
▪️ Extensive **glomerulosclerosis or interstitial fibrosis** on biopsy
146
# IgA nephropathy
What **urine findings** are typical in IgA nephropathy⁉️
* **Red blood cell (RBC) casts**
🔬 **Dysmorphic RBCs**
🧪 Proteinuria may be present
147
# IgA nephropathy
What is the **long-term prognosis** of IgA nephropathy⁉️
📉 Outcome over 25 years:
▪️ **~30%** → spontaneous **remission**
▪️ **~30%**→ progress to **ESRD**
▪️ **Remaining** → **persistent hematuria with normal renal function**
| ESRD : End-stage renal disease
148
# IgA nephropathy
How does **hemolytic uremic syndrome** (HUS) differ from **IgA nephropathy**⁉️
🆚 **HUS**:
▪️ Affects **younger children**
▪️ **Preceded by GI infection** (e.g., E. coli O157:H7)
▪️ Presents with:
- Abdominal pain
- Bloody diarrhea
- **Systemic symptoms** (fever, lethargy)
▪️ Labs: Hemolytic anemia, thrombocytopenia, AKI
🆚 **IgA Nephropathy**:
▪️ Affects **older children**/adults
▪️ **Triggered by URTI**
▪️ Presents with **macrohematuria, often without systemic illness**
149
# IgA nephropathy
How is IgA nephropathy **managed** **based on presentation⁉️**
📌 **Based on severity**:
1️⃣ **Asymptomatic microhematuria** → **Follow-up** only
2️⃣ **Proteinuria or declining GFR** → ✅ **ACE inhibitors**
3️⃣ **RPGN (rapidly progressive GN**) → **Steroids** + **cytotoxic agents** + **plasmapheresis**
150
# Autosomal Dominant Polycystic Kidney Disease (ADPKD):
What **classic triad** suggests a diagnosis of **ADPKD** in a young patient⁉️
| Autosomal Dominant Polycystic Kidney Disease (ADPKD):
🧠 ADPKD should be suspected in:
▪️ **Hematuria**
▪️ **Renal cysts on ultrasound**
▪️ **Family history** of end-stage renal disease (ESRD)
151
# Autosomal Dominant Polycystic Kidney Disease (ADPKD
What **causes autosomal dominant polycystic kidney disease** (ADPKD) and what is its renal impact⁉️
🧬 Caused by **PKD gene mutation**
➡️ Leads to multiple renal cysts
152
Which **vascular abnormality** is characteristic of ADPKD⁉️
🧠 **Berry aneurysm** (not aortic aneurysm)
✅ ↑ Risk of **subarachnoid hemorrhage**, especially with **family history**
153
How do **ADPKD renal cysts **differ from **medullary cystic disease⁉️**
🧬 In **ADPKD**, **cysts occur in both cortex and medulla**
➡️ **Genetic mutation** differs from **medullary cystic kidney disease**, which is **autosomal dominant tubulointerstitial disease**
154
# Autosomal Dominant Polycystic Kidney Disease (ADPKD)
What is the **most common presenting symptom** of ADPKD⁉️
* 📍 **Back or hip pain**
🧠 Due to:
▪️ Cyst **rupture or hemorrhage**
▪️ Cyst **infection**
▪️ **Nephrolithiasis**
155
# Autosomal Dominant Polycystic Kidney Disease (ADPKD)
What are the **renal and systemic complications** of ADPKD⁉️
1. 🚩 **Renal**:
▪️ **Hypertension** ✅
▪️ **Hematuria**
▪️ **Cyst infections**
▪️ **Nephrolithiasis**
▪️ **ESRD** (>50% by late middle age)
2. **Systemic**:
▪️ **Berry aneurysms** (↑ risk 4–5×)
▪️ **Mitral valve prolapse**, **aortic/tricuspid insufficiency**
▪️ **Hernias**, **diverticulosis**, **liver cysts**
156
# Autosomal Dominant Polycystic Kidney Disease (ADPKD)
How is **ADPKD diagnosed** in young patients (**15–29 years old**)⁉️
* **≥2 renal cysts** (unilateral or bilateral) **+** **positive family history**
📈 **Sensitivity = 96%, Specificity = 100%**
* **note:** **older patients require more cysts on imaging to confidently diagnose ADPKD**
157
# Autosomal Dominant Polycystic Kidney Disease (ADPKD
How is ADPKD diagnosed using **imaging** and **age-based criteria**⁉️
🔬 Diagnosis via **ultrasound** + **family history**
📅 **Cyst** criteria by age:
✅ **Age 15–29:** **≥2 cysts** (uni- or bilaterally)
✅ Age **30–59**: **≥4 cysts** total
158
# Autosomal Dominant Polycystic Kidney Disease (ADPKD)
Is **liver failure** associated with ADPKD⁉️
**NO**,Liver cysts may occur, **but liver failure is rare**
159
# Autosomal Dominant Polycystic Kidney Disease (ADPKD)
hat **cerebrovascular complication** is associated with ADPKD⁉️
🧠 **Intracerebral (Berry) aneurysms**
📈 Occur **4–5× more frequently** than in the general population
160
What defines **microalbuminuria** and why is it important in diabetic patients⁉️
* Microalbuminuria = **30–300** mg/day of albumin excretion
* 🧠 **Indicates** **early diabetic nephropathy**
➡️ Requires **regular screening in diabetic patients** for early detection and intervention
161
# diabetic nephropathy
What is the **classic histological finding** in diabetic nephropathy⁉️
🧬 **Nodular glomerulosclerosis** (**Kimmelstiel-Wilson nodules)**
* 📍 **Due to mesangial matrix expansion from long-standing hyperglycemia**
162
# diabetic nephropathy
hat is the most appropriate **first-line drug** to **reduce albuminuria** and **protect renal function** in **diabetic nephropathy⁉️**
✅ **ACE inhibitors** (e.g. **Ramipril**)
🧠 Benefits:
▪️ Reduces **albuminuria**
▪️ **Slows progression** to ESRD
▪️ Provides **BP control**
163
# diabetic nephropathy
What is the **natural progression** of diabetic nephropathy⁉️
* 📈 **Timeline**:
1️⃣ **0–5 yrs**: Glomerular **hyperfiltration**, renal **hypertrophy**
2️⃣ **5–10 yrs**: **Microalbuminuria** (30–300 mg/day)
3️⃣ **~15 yrs**: **Proteinuria** (>300 mg/day)
⚠️ **~50% with proteinuria → ESRD within 5–10 years**
164
# diabetic nephropathy
What is the **primary treatment goal** in diabetic nephropathy⁉️
🎯 **Prevent** the onset or progression of **proteinuria**
🧠 **Once significant proteinuria appears, renal function decline is harder to stop.**
165
# diabetic nephropathy
What are the **main strategies** to **prevent progression** of diabetic nephropathy⁉️
🛡️ Protective measures include:
▪️ ✅ Tight **glucose** control
▪️ ✅ **Blood pressure** control
▪️ ✅ RAAS blockade: **ACE inhibitors** or **ARBs**
▪️ ✅ **SGLT2 inhibitors** ➡️ reduce proteinuria and preserve renal function
✅ **Dietary modifications**:
* Salt restriction
* Protein restriction
166
How do you **prevent continuous polyuria** after relieving hydronephrosis⁉️
💧 Administer **IV fluids in a lower amount than urine output**
🧠 **Prevents ongoing post-obstructive diuresis**
📍 Requires **close monitoring** of **fluid balance** and **electrolytes**
167
How is **albuminuria** classified in diabetic nephropathy⁉️
* ✅ **Microalbuminuria**:
* 30–300 mg/day
* Spot albumin:creatinine ratio (ACR) >30 mg/g
* ✅ **Macroalbuminuria**:*
* >300 mg/day
168
Why is **albuminuria clinically significant** in **diabetes**⁉️
🚨 Albuminuria is a risk factor for:
✅ **Cardiovascular disease**
✅ **Chronic kidney disease** (CKD)
169
When should **screening** for **microalbuminuria** be done in patients with **diabetes mellitus⁉️**
📅 **Type 2 DM**: **At diagnosis**, then **yearly**
📅 **Type 1 DM**: **Start 5 years after diagnosis**, then **yearly**
170
# reflux nephropathy
❓What is **reflux nephropathy** and how does it **develop**⁉️
* 🧠 **Reflux nephropathy** is **chronic kidney damage**
* caused by **vesicoureteral reflux (VUR) OR other urologic anomalies** in **early childhood**
* 📍 Leads to **recurrent UTIs**, **renal scarring**, and **eventual CKD (**chronic kidney disease)
171
# reflux nephropathy
What **clinical history** suggests reflux nephropathy in an adult⁉️
* 📍 **History** of:
▪️ Recurrent childhood **UTIs**
▪️ Prolonged **bed-wetting**
* 🧪 **Now** Often **asymptomatic in adulthood** OR presenting with :
▪️ **Hypertension**
▪️ Mild to moderate **proteinuria**
▪️ **CKD** with **unremarkable urine sediment**
172
How is reflux nephropathy **diagnosed** in **childhood**?
* ✔️ **Vesicoureteral reflux (VUR)** is diagnosed using **renal ultrasound** or **voiding cystourethrogram (VCUG)**
* ✔️ **Recurrent UTIs may raise suspicion early on in childhood 🧬**
173
# reflux nephropathy
What are the classic **ultrasound findings** in adult reflux nephropathy⁉️
* Renal ultrasound shows:
▪️ **Asymmetric** **small** kidneys
▪️ **Irregular renal outlines**
▪️ **Thinned cortices**
▪️ **Regions of compensatory hypertrophy (enlarged areas in response to damage) 💪**
174
# reflux nephropathy
How is reflux nephropathy **managed** in **children** and **adults**⁉️
1. 🧒🏼 **In children (before scarring):**
▪️ Consider **surgical correction** for high-grade VUR
▪️ Aim: **prevent recurrent UTIs and scarring**
🧑 2. **In adults**:
▪️ Focus on **strict blood pressure control**
▪️ ✅ Use **ACE inhibitors** or **ARBs** to **slow CKD progression and reduce proteinuria**
175
# reflux nephropathy
Which **nephrotoxic drugs** commonly cause **acute tubular necrosis (ATN**)⁉️
* 🧪 **Aminoglycosides**
* 🧪 **Amphotericin** B
📍 Both cause **intrinsic AKI** due to **direct tubular damage**
176
# Drug induced AKI
What are the **key features** of **aminoglycoside**-induced AKI⁉️
▪️ Onset: **5–7 days after initiation**
▪️ **Non-oliguric AKI**
▪️ **Hypomagnesemia**
▪️ May **progress even after stopping the drug**
177
# Drug induced AKI
Which **nephrotoxic drug** is classically associated with **non-oliguric acute kidney injury**⁉️
✅ **Aminoglycosides** (e.g., **amikacin**)
🧪 **Urine output remains >400** mL/day **despite tubular damage**
178
# Drug induced AKI
What are the **key features** of **amphotericin** B–induced AKI⁉️
💧
* ▪️ **Polyuria**
* ▪️ **Hypomagnesemia, hypocalcemia**
* ▪️ Non-anion gap **metabolic acidosis**
Due to **distal tubular injury**
179
# Drug induced AKI
How do **aminoglycosides cause acute kidney injury⁉️**
🧪 **Intrinsic AKI** due to **acute tubular necrosis** (ATN)
🧠 Key features:
▪️ **Muddy brown casts in urine**
▪️ **Non-oliguric AKI**
▪️ **Hypomagnesemia**
📍 Categorized under:
🔻 **Renal** → **Tubular** → **Nephrotoxins** → **Exogenous** → **Aminoglycoside**
180
# Goodpasture's disease
What is the **immunofluorescence finding** in Goodpasture's disease⁉️
💡 **Linear IgG deposits** **along the glomerular basement membrane**
181
# Goodpasture's disease
❓What are the **renal** **side effects** of **Amphotericin** B⁉️
🧪 Causes **intrinsic AKI** due to acute tubular necrosis (ATN)
📍 Classic findings:
▪️ **Polyuria**
▪️ **Hypomagnesemia**
▪️ **Hypocalcemia**
▪️ Non-anion gap **metabolic acidosis**
🧠 Mechanism: **Distal tubular damage** + **electrolyte wasting**
182
# Goodpasture’s disease
What is **Goodpasture’s disease**, and what are its **hallmark features**⁉️
🫁🩸 **Goodpasture’s disease** = **pulmonary-renal syndrome**
🧠 Caused by **anti-glomerular basement membrane** (anti-GBM) **antibodies**
📍 Classic presentation:
▪️ **Hematuria** (**renal** involvement)
▪️ **Hemoptysis** (**lung** involvement)
183
# Goodpasture’s disease
What is Goodpasture's disease **characterized by⁉️**
🧠 **Antibodies against the glomerular basement membrane (anti-GBM)**
🫁➡️ Causes **glomerulonephritis** and **hemoptysis** (lung injury)
184
# Goodpasture’s disease
What is seen on **kidney biopsy** in Goodpasture’s disease⁉️
* Necrotizing and **crescentic glomerulonephritis**
✅ **Linear IgG** staining on immunofluorescence ➡️ **diagnostic for anti-GBM disease**
185
# Goodpasture’s disease
How is Goodpasture’s disease **treated**⁉️
* 💉 **Plasmapheresis** to remove anti-GBM antibodies
💊 Plus **oral prednisone** and **cyclophosphamide** for immunosuppression
* 📆 **Treatment is most effective early in the disease course**
186
# Goodpasture’s disease
How does Goodpasture’s disease **differ** from **granulomatosis with polyangiitis (Wegener's**)⁉️
❌ Wegener's has **negative immunofluorescence** and upper/lower respiratory symptoms
✅ Goodpasture's has **linear IgG deposits**
187
What is **the most common type of cancer** in **kidney transplant recipients**⁉️
✅ **Skin and lip cancers** , **non-Hodgkin lymphoma**, and **cervical carcinoma in situ**
📈 Occur due to **lifelong immunosuppressive therapy**
🧠 Risk of malignancy is **~100× higher than in the general population of the same age**
188
Why are kidney transplant recipients at **increased cancer risk**⁉️
💊Due to **Chronic immunosuppression suppresses** immune surveillance against:
▪️ Malignant cells
▪️ Viruses (e.g., EBV ➡️ post-transplant lymphoproliferative disease)
189
What is **post-transplant lymphoproliferative disorder** (PTLD), and **when does it occur⁉️**
* **B-cell proliferation disorder** (often **EBV-driven**)
* 📍 Can occur early (< 1 year) or late (7–10 years) post-transplant
* 📌 **Risk ↑ with intensity of immunosuppression**
190
What is the **initial test** for **suspected primary hyperaldosteronism** in patients with **resistant hypertension⁉️**
🧪 **Aldosterone:Renin Ratio (ARR)**
🧠 Used to **screen for primary hyperaldosteronism**
* 📍 **Indicated** in patients with:
▪️ **Resistant hypertension**
▪️ **Hypokalemia**
▪️ **Adrenal incidentaloma**
191
hat are the **classic clinical manifestations** of **primary hyperaldosteronism⁉️**
* Due to **excess aldosterone** ➡️ **renal K⁺ loss and Na⁺ retention**
* 📍 Features:
▪️ **Hypertension** (often **resistant**)
▪️ **Hypokalemia**
▪️ **Hypernatremia**
▪️ **Metabolic alkalosis**
▪️ **Muscle weakness**, **cramps**, **proximal myopathy**
192
When should **hypertensive patients** be **screened for primary hyperaldosteronism⁉️**
* ✅ = Indications to check *Aldosterone:Renin Ratio (ARR):*
▪️ **Resistant hypertension** (uncontrolled on ≥3 drugs)
▪️ **Hypokalemia**
▪️ **Adrenal mass**
▪️ **Age of onset < 40 years**
193
When should you **suspect** mineralocorticoid excess (**primary hyperaldosteronism)⁉️**
📍 In patients with **hypertension** + **any**of the following:
▪️ **Drug-resistant hypertension (≥3 meds**)
▪️ Spontaneous or diuretic-induced **hypokalemia**
▪️ **Adrenal mass**
▪️ **Onset < 40 years**, **family history** of early HTN or stroke
194
What **defines** a **positive aldosterone:renin ratio (ARR)** in screening for primary hyperaldosteronism⁉️
* **ARR >750 pmol/L**
AND **aldosterone >450 pmol/L**
* 📌 **Must correct hypokalemia before testing**
195
What is the **next diagnostic step** after **confirming primary hyperaldosteronism⁉️**
🖥️ **Adrenal CT scan** to **localize the lesion**
* 📍 If **no lesion** or **unilateral lesion in age >40:**
➡️ **Adrenal vein sampling**
196
What **imaging** is used to **localize the lesion⁉️**
🖥️ **Unenhanced adrenal CT scan**
▪️ Detects **unilateral adenoma**, **bilateral hyperplasia**, or **normal** **adrenal morphology**
197
What **confirmatory tests** are used **after a positive ARR⁉️**
* 📍 Confirmation with **suppression testing**:
1. **Saline infusion test**
2. **Oral sodium loading**
3. **Fludrocortisone suppression test**
198
How is **primary hyperaldosteronism** ***treated***⁉️
🧑⚕️ **Surgical if unilateral adenoma**
💊 **Pharmacologic** if **bilateral hyperplasia** or non-surgical:
➡️ **Spironolactone** (**aldosterone antagonist**)
199
Which medications **must be stopped** **before measuring the aldosterone:renin ratio (ARR**)⁉️
* ✅ Only **mineralocorticoid receptor antagonists** (e.g., Spironolactone, eplerenone)
* 📆 Stop **at least 4 weeks before testing**
* 🧠 **They falsely elevate renin, leading to inaccurate results**
200
What is **acute interstitial nephritis** (AIN), and what are its **common causes**⁉️
🧠 **AIN** = **inflammation of the renal interstitium** & **tubules**, **leading to acute kidney injury**
📆 **Onset**: Days to weeks
🔹 **Common causes**:
1️⃣ **Drugs (most common):**
▪️ Penicillins, Rifampin
▪️ Proton pump inhibitors (PPIs)
▪️ Sulfonamides
2️⃣ **Infections**:
▪️ Mycoplasma
▪️ CMV, EBV
3️⃣ **Systemic diseases**:
▪️ Sarcoidosis
▪️ Sjögren’s syndrome
▪️ Systemic lupus erythematosus (SLE)
201
# acute interstitial nephritis (AIN)
What are the **classic clinical features** of **acute interstitial nephritis (AIN)⁉️**
🧠 **Classic triad**:
▪️ **Fever**
▪️ **Rash**
▪️ **Peripheral eosinophilia**
➕ **Oliguric acute kidney injury** (AKI)
202
# acute interstitial nephritis (AIN)
What is **acute interstitial nephritis (AIN) and what causes it⁉️**
* Interstitial nephritis is a syndrome of:
▪️ **Acute kidney failure**
▪️ **Rash** 🌸
▪️ **Fever** 🌡️
▪️ **Arthritis**
▪️ **Peripheral eosinophilia**
▪️ **Eosinophiluria**
➡️ Often **triggered by drugs** (e.g., antibiotics, PPIs, NSAIDs)
203
# acute interstitial nephritis (AIN)
❓What is the **treatment of acute interstitial nephritis (AIN)⁉️**
1️⃣ **Stop the offending agent immediately**
2️⃣ **Glucocorticoids** if:
▪️ **AIN due to systemic disease (absolute indication)** OR **Worsening AKI or dialysis needed (relative indication)**
204
# acute interstitial nephritis (AIN)
When is **glucocorticoid therapy indicated** in acute interstitial nephritis (AIN)⁉️
🩺 **Absolute indications**:
➡️ AIN **secondary to systemic disease:**
▪️ Sjögren’s syndrome
▪️ Sarcoidosis
▪️ SLE nephritis
▪️ Tubulointerstitial nephritis with uveitis
▪️ Idiopathic interstitial nephritis
🩺 **Relative indications**:
➡️ Drug-induced AIN with:
▪️ **Rapid decline in renal function**
▪️ **Impending need for dialysis**
205
# acute interstitial nephritis (AIN)
What are **key urine findings** in AIN⁉️
▪️ **WBC casts**
▪️ **Hematuria**
▪️ **Pyuria**
▪️ **± Eosinophiluria**
206
# acute interstitial nephritis (AIN)
What is the **most common presentation** of AIN⁉️
🧪 **Renal failure** with or without eosinophiluria (partial presentation is more common than full triad)
207
# acute interstitial nephritis (AIN)
❓What is the **prognosis** of AIN after drug discontinuation⁉️
✅ **Usually good**—most patients recover without permanent kidney damage
208
# acute interstitial nephritis (AIN)
How is AIN **diagnosed**⁉️
* 📍 **Clues**:
▪️ Recent drug exposure or systemic illness
▪️ Unexplained renal failure
* 🧪 **Urinalysis**:
▪️ WBC casts
▪️ Pyuria
▪️ Hematuria
▪️ Urine eosinophils (not specific)
209
# ****
What is the definition of **sarcoidosis**⁉️
Sarcoidosis = **multisystem inflammatory granulomatous disorder** of **unknown cause**, **defined by non-caseating granulomas**
210
# sarcoidosis
What is the **pathological hallmark** of sarcoidosis⁉️
🔬 ✅ **Granuloma (non-caseating**)
⚠️ Nonspecific but essential for diagnosis
211
# sarcoidosis
What are the **special clinical forms** of sarcoidosis⁉️
🔹 **Löfgren’s syndrome:**
▪️ Erythema nodosum + bilateral hilar adenopathy + migratory polyarthritis
🧠 Good prognosis
🔹 **Lupus pernio:**
▪️ Purple facial lesions (bridge of nose, cheeks)
🧠 Pathognomonic
🔹 **Heerfordt syndrome:** triad of :
▪️ Parotitis + uveitis + facial palsy
212
# sarcoidosis
What is the **typical presentation** of sarcoidosis⁉️
* 🧍♂️ **Multisystem**; varies from **asymptomatic to organ failure**
🫁 **Lungs**: Bilateral hilar adenopathy, interstitial disease
👀 **Eyes**: Uveitis, retinitis
🧠 **CNS**: CN VII palsy, myelopathy
🦴 **Musculoskeletal**: Myalgias, arthralgia
🧬 **Bone marrow/spleen**: Anemia, splenomegaly
🧫 **Skin**: Erythema nodosum, plaques
🧬 **Kidney**: **Nephritis, stones**
🫀 **Cardiac**: Arrhythmia, heart block
🦴 **Calcium**: **Hypercalcemia** (via granuloma-mediated Vit D)
213
# sarcoidosis
What is the best **initial test** for **diagnosing** sarcoidosis⁉️
🩻 ✅ **Chest X-ray**
➡️ **Detects bilateral hilar lymphadenopathy**
214
# sarcoidosis
What is the **gold standard for diagnosing** sarcoidosis⁉️
🧪 ✅ **Biopsy** showing **non-caseating granulomas**
🔍 Done when no alternative diagnosis is identified
215
# sarcoidosis
What are the **typical lab findings** in sarcoidosis⁉️
🧪 ⬆️ **ACE level**
🧪 ⬆️ **CD4:CD8 ratio**
🧪 ⬆️ **Inflammatory markers**
🧪 ⬆️ **Calcium**
216
# sarcoidosis
What are the **stages** of sarcoidosis **based on chest X-ray findings⁉️**
* **Stage 1**: **Hilar lymphadenopathy**
* **Stage 2**: **Adenopathy + infiltrates**
* **Stage 3**: **Infiltrates only**
* **Stage 4**: Lung **fibrosis**
217
# sarcoidosis
What is the **treatment for acute sarcoidosis**⁉️
✅ **Mild/no symptoms** → **No** treatment
✅ **Single organ** → **Topical** steroids
✅ **Multi-organ or systemic** → **Systemic** steroids
218
# sarcoidosis
What is the **treatment for chronic sarcoidosis⁉️**
💊 GCS **tolerated** ➡️ < 10 mg/d prednisone
💊 GCS **not tolerated** ➡️ Methotrexate, Hydroxychloroquine, Azathioprine, Leflunomide
💊 **Refractory cases** ➡️ Infliximab, Cyclophosphamide, Thalidomide
| glucocorticosteroids (GCs)
219
# sarcoidosis
Which organ is **most commonly** involved in sarcoidosis & w**hy is chest X-ray diagnostic**⁉️
* 🫁 **Lungs**
**Involved in >90% of patients**
* 📍 **Chest X-ray detects hilar lymphadenopathy & fibrosis, making it the best initial test**
220
What is the **typical cause** of **post-streptococcal glomerulonephritis** (PSGN)⁉️
🧫 **Immune complex–mediated glomerulonephritis**
➡️ **Follows infection** with nephritogenic strains of **group A streptococci**
221
# Poststreptococcal Glomerulonephritis (PSGN)
What are the **key clinical features** of Poststreptococcal Glomerulonephritis (PSGN)?
🧒🏻 Occurs
* **1–3 weeks after pharyngitis**
* or **2–6 weeks after skin infection** with **Group A Streptococcus**
📍 Presents as **nephritic syndrome**:
* **Hematuria** (cola-colored urine)
* **RBC casts, pyuria**
* Mild-moderate **proteinuria**
* **Hypertension**
222
# Poststreptococcal Glomerulonephritis (PSGN)
What **systemic symptoms** are associated with PSGN⁉️
▪️ **Headache**
▪️ **Malaise**
▪️ **Anorexia**
▪️ **Flank pain**
223
# Poststreptococcal Glomerulonephritis (PSGN)
What are the **diagnostic and lab findings in PSGN⁉️**
* 🔬 **Biopsy**:
▪️ **Subendothelial + subepithelial deposits of IgG, IgM, and complement**
* 🧪 **Labs:**
▪️ ⬇️ **CH50 and C3**
▪️ ✅ **Normal C4**
▪️ ⬆️ **ASO and anti-DNase B titers**
224
# Poststreptococcal Glomerulonephritis (PSGN)
What is the **treatment** for PSGN⁉️
* 1. **Supportive care**:
▪️ Control **hypertension & edema**
▪️ **Dialysis** if **renal failure is severe or unresponsive**
* 2. Antibiotics **Penicillin** for **patient** & **close contacts** to eradicate Group A Streptococcus
* ❌ Immunosuppressants are not used in PSGN
225
What is the typical **complement pattern** in Poststreptococcal Glomerulonephritis (PSGN) , and the perentage of ocuurance ⁉️
🧪 ✅ **Decreased C3**
🧪 ✅ **Normal C4**
📊 **Seen in ~90% of PSGN cases**
🧠 Due to **activation of the alternative complement pathway**
226
# lupus nephritis
What is **the most serious manifestation** of systemic lupus erythematosus (SLE)⁉️
🧠 **Lupus nephritis**
⚠️ Alongside infection, it is a leading cause of early mortality in SLE
227
# lupus nephritis
What are the **key clinical features** of proliferative lupus nephritis⁉️
🔬 **Microscopic hematuria**
🔬 **Proteinuria >500** mg/24h
🩺 **Hypertension**
📈 **Elevated creatinine**
⛔ **Nephrotic syndrome in ~50% of cases**
228
# lupus nephritis
What is the initial **treatment for severe or life-threatening lupus nephritis**⁉️
💉 **IV corticosteroids + cyclophosphamide**
💊 **Mycophenolate mofetil** (MMF) is an **alternative** ➕ May **combine MMF** with calcineurin inhibitors (e.g. tacrolimus)
229
# lupus nephritis
Is **renal biopsy** required before starting treatment in severe lupus nephritis⁉️
🚫 **No** — Do not delay treatment
Initiate glucocorticoids immediately in organ-threatening disease
230
# lupus nephritis
When is **plasmapheresis** used in SLE⁉️
❌ **Not standard treatment for lupus nephritis**
✅ Reserved for severe hematologic or neurologic involvement (e.g. TTP, catastrophic APS)
231
What type of **renal stone** is associated with **urease-positive bacterial infections⁉️**
✅ **Struvite stones** (**magnesium ammonium phosphate**)
🦠 Caused by urease-positive organisms like **Proteus, Klebsiella, Providencia**
➡️ **Urease ↑ urine pH > 8** ➕ **ammonium production**
232
Which renal stone **type forms staghorn calculi** and **thrives in alkaline urine**⁉️
* 🧱 **Struvite stones**
🧪 **Alkaline urine (pH > 8**)
📍 Often **fill the renal pelvis** → **Staghorn calculi**
233
Which **bacteria are urease-positive and contribute to struvite stone formation**⁉️
🦠 **Proteus**, **Klebsiella**, **Providencia**
⛔ E. coli, Enterococcus, and other urease-negative bacteria do not cause struvite stones
234
# Minimal Change Disease (MCD)
What is the **first-line treatment** for the first recurrence of **Minimal Change Disease (MCD)⁉️**
* 💊 **Steroids**
* 🧠 Other immunosuppressants (e.g., cyclophosphamide, MMF) are reserved for:
▪️ **Multiple recurrences**
▪️ **Steroid resistance**
▪️ **Steroid dependence**
235
# Minimal Change Disease (MCD)
What **percentage of children** with MCD **experience recurrence**⁉️
📊 **70–75%** of children **have at least one recurrence**
⚠️ Recurrence is less common in adults
236
# Minimal Change Disease (MCD)
What are the **key features** of **Minimal Change Disease (MCD)⁉️**
▪️ **Massive proteinuria**
▪️ **Hypoalbuminemia**
▪️ **Edema**
▪️ ± **Hypertension** (more in adults)
▪️ ± **Atopic symptoms** (more in children)
237
# Minimal Change Disease (MCD)
What are the **biopsy** findings in MCD⁉️
▪️ **Normal** glomeruli on **light microscopy**
▪️ Negative immunofluorescence
▪️ **Podocyte effacement** on **electron microscopy**
238
# Minimal Change Disease (MCD)
When should a **repeat biopsy** be considered in MCD⁉️
🧠 In **steroid-unresponsive cases**
➡️ **To rule out Focal Segmental Glomerulosclerosis (FSGS**)
239
Which common GI condition causes **non-anion gap metabolic acidosis⁉️**
**Diarrhea** → Loss of HCO₃⁻ → **Normal anion gap acidosis**
240
What is the **dialysis access** method with the **lowest risk of infection⁉️**
✅ **Arteriovenous (AV) fistula**
🧠 Surgically **connects an artery to a vein**
💪 **Increases blood flow** → vein enlarges and strengthens
➡️ **Preferred long-term access for hemodialysis**
241
Why is an **AV fistula** **not suitable** for **urgent dialysis⁉️**
* 🕒 It requires **weeks to mature**
* ❌ Not ideal for **immediate/acute dialysis needs**
242
What are **common sites** for **AV fistula creation⁉️**
* 📍 **Wrist** → Radiocephalic fistula
* 📍 **Elbow** → Brachiocephalic fistula
243
**Rank dialysis** **access** sites by infection risk (**highest to lowest)⁉️**
1️⃣ **Femoral vein catheter** – 🚨 **Highest infection risk**
2️⃣ **Internal jugular vein**
3️⃣ **Subclavian vein** – 💉 Lowest among central lines
4️⃣ **AV fistula **– ✅ Lowest overall
244
Which dialysis access site carries the **highest risk of infection**⁉️
1️⃣ **Femoral vein catheter**
245
What are the **main causes of anemia** in CKD patients⁉️
🔑🧠 **mnemonic** **"I HELP RBCs FAIL"**
🅘 — **Iron deficiency** (GI loss, poor intake)
🅗 — **Hyperparathyroidism** → marrow fibrosis
🅔 — **Erythropoietin deficiency** (primary cause)
🅛 — **Low RBC survival**
🅟 — **Pregnancy & comorbidities** (thyroid disorders, HIV, autoimmune disease)
🅡 — **RBC bleeding diathesis**
🅑 — **B12 or folate deficiency**
🅒 — **Chronic inflammation**
🅢 — **Sickle cell & other hemoglobinopathies**
🅕 — **Failure due to immunosuppressive drugs**
246
What are the key **side effects** of **thiazide diuretics**, and **how can they benefit certain kidney patients⁉️**
* 🧪 Side effects of thiazides:
⬇️ **Hyponatremia**
⬇️ **Hypokalemia**
⬆️ **Hyperuricemia**
⬆️ **Hypercalcemia** ✅
* Clinical benefit:
➡️ **↓ Urinary calcium excretion (hypocalciuria)**
➡️ ✅ **Suitable for patients with recurrent nephrolithiasis** and **hypertension**
247
What **antihypertensive** is preferred in patients with **recurrent calcium oxalate stones**⁉️
✅ **Thiazide diuretics** → **lower BP** and **prevent calcium stone formation**
explanation :
* ➡️ **↓ Urinary calcium excretion (hypocalciuria)**
➡️ ✅ **Suitable for patients with recurrent nephrolithiasis** and **hypertension**
248
What is the likely cause of **acute renal failure** after starting **ACE inhibitors** in a patient with **diffuse atherosclerosis and peripheral arterial disease⁉️**
**Renal artery stenosis** due to atherosclerosis (**renovascular hypertension**)
➡️ ACE inhibitors (e.g., ramipril) dilate the efferent arteriole
➡️ This reduces glomerular filtration pressure and can cause acute renal failure
249
What are the key **electrolyte and lab abnormalities** seen in **ACE inhibitor–induced renal failure in renovascular hypertension⁉️**
🔻 Borderline **hyponatremia**
🔺 **Hyperkalemia**
📈 Rising **serum creatinine**
250
What is the immediate **management** of **suspected ACE inhibitor–induced acute renal failure** due to renal artery stenosis⁉️
🚩 **Stop** the ACE inhibitor immediately
📍 **Monitor serial serum potassium** and **creatinine**
251
What are the **imaging** and **interventional** options for **suspected renal artery stenosis**⁉️
* **Diagnostic imaging**:
**Renal Doppler ultrasound**
**CT angiography**
**MR angiography**
* 💉 **Interventions**:
▪️ **Percutaneous transluminal renal angioplasty (PTRA**)
▪️ **Vascular stent** placement
▪️ **Surgical renal revascularization**
252
When should **renovascular hypertension be suspected** in clinical practice⁉️
🧠 Suspect renovascular hypertension in:
🔻 **Patients with atherosclerotic vascular disease** ➕
🔻 **Unexplained renal function deterioration** OR
🔻 **Worsening renal function after ACE inhibitor** (e.g., ramipril)
253
What is the **first step in evaluating the cause of hyponatremia**⁉️
🩺 **Assess volume status** via:
✅ **Physical exam** (e.g., JVP, BP, skin turgor)
✅ **Urine osmolality**
✅ **Urine sodium concentration**
254
What is the **stepwise diagnostic approach** to a patient with **hyponatremia** (Na⁺ < 135)⁉️
A:
🧪 Stepwise approach:
➡️ Step 1: Check **plasma osmolality**
* Normal/high ➡️ Pseudohyponatremia
* Low (< 280) ➡️ Hypotonic hyponatremia
➡️ Step 2: Assess **volume status**
* Hypovolemic
* Euvolemic
* Hypervolemic
255
What are the causes of **hypovolemic hyponatremia** based on urine sodium levels (Una)⁉️
🚩 **Una < 20** (**extrarenal losses**):
* Dehydration
* Vomiting
* Diarrhea
* Third spacing
🚩 **Una > 20** (**renal losses**):
* Diuretics
* Mineralocorticoid deficiency
* Cerebral salt wasting
256
What are the common causes of **euvolemic hyponatremia**⁉️
✅ SIADH
✅ Hypothyroidism
✅ Glucocorticoid deficiency
✅ Psychogenic polydipsia
✅ Low solute intake ("tea & toast" diet)
257
What **physical signs suggest hypovolemia** as a cause of hyponatremia⁉️
* **Signs of dehydration (hypovolemia):**
🔻 Low blood pressure
🔻 Orthostatic hypotension
🔻 Low skin turgor
🔻 Reduced jugular venous pressure (JVP)
258
How does **urine osmolality** help differentiate between causes of hyponatremia⁉️
📊 Urine osmolality:
✅ **>400** mOsm/kg ➡️ **SIADH**
✅ **< 100** mOsm/kg ➡️ **Primary polydipsia**
🔄 **100–400** mOsm/kg ➡️ **Mixed/combined disorders**
259
How does **urine sodium concentration** help distinguish between causes of hyponatremia⁉️
* 🧪 **Low urine Na⁺ (< 20 mEq):** ➡️ Dehydration (kidneys retain Na⁺ to preserve volume)
* 🧪 **High urine Na⁺ (>20–30 mEq):** ➡️ SIADH or renal salt-wasting
260
What **urine findings** suggest **dehydration as the cause of hyponatremia**⁉️
🧪 **Decreased** **urine sodium concentration** ➕
📈 **Elevated urine osmolarity**
➡️ These findings indicate hypovolemia/dehydration as the underlying cause
261
What does the acronym **CRAB** stand for in **multiple myeloma** (MM)⁉️
🦀 CRAB = classic features of MM:
✅ **C** – **HyperCalcemia** (due to osteolysis)
✅ **R** – **Renal failure** (e.g., cast nephropathy)
✅ **A** – **Anemia** (normocytic, normochromic)
✅ **B** – **Bone disease** (lytic lesions)
262
What are the **diagnostic criteria** for **multiple myeloma (MM**)⁉️
🧪 Diagnosis requires:
1️⃣ **Bone marrow plasma cells >10%**
2️⃣ **M-protein in serum/urine**(electrophoresis)
3️⃣ **At least one myeloma-defining event**:
* CRAB features
* BM plasma cells >60%
* >1 focal lesion on MRI
* Light chain ratio ≥100 (involved:uninvolved)
263
What is the **renal complication** of MM and how is it detected⁉️
🚨 **Cast nephropathy** = classic MM renal injury
➡️ Caused by **light chains** binding Tamm-Horsfall protein in tubules
⛔ **Urine dipstick is negative** (detects albumin, not light chains)
✅ Detected via **24h urine collection for Bence-Jones proteins**
264
Why can a patient with MM have **high proteinuria** but a **negative dipstick**⁉️
⛔ Dipstick detects **albumin**, but MM causes light **chain proteinuria**
➡️ Needs **urine protein electrophoresis** or **24h urine collection**
265
Why is **pre-renal AKI unlikely in MM-related kidney injury**⁉️
❌ MM typically causes **intrinsic AKI** (cast nephropathy)
❌ No signs of volume depletion or hypoperfusion in the scenario
266
What is the **link** between **diabetic nephropathy** and **retinopathy**⁉️
* 🧠 **Diabetic retinopathy is commonly seen with nephropathy**
* ✅ **All patients with diabetic nephropathy should be screened for retinopathy**
➡️ Prevents progression to blindness
267
What type of **acute kidney injury** (AKI) is caused by **benign prostatic hyperplasia** (BPH)⁉️ and how ttt ?
* 🚫 **Post-renal AKI**
✅ Due to **bladder outlet obstruction** from BPH
✅ Presents with **urinary retention, ↓ urine output, and ↑ creatinine**
✅ Immediate treatment: Insert a urinary catheter
268
What **electrolyte abnormality** is commonly seen in AKI caused by **aminoglycosides**⁉️
**Hypomagnesemia**
✅ Common in aminoglycoside-induced acute tubular necrosis (ATN)
✅ Due to **renal magnesium wasting**
269
What is **uremic pericarditis** and in **which condition does it occur⁉️**
🧠 Uremic pericarditis is a **complication of end-stage renal disease (ESRD)**
➡️ Caused by **toxic accumulation of uremic metabolites**
➡️ May **progress** to **cardiac tamponade if untreated**
270
What is the **definitive treatment** for **uremic pericarditis**⁉️
💊 **Urgent dialysis without heparin**
✅ **Heparin** is **withheld** to **avoid risk of hemorrhagic** **pericardial effusion**
271
What is the **emergency management** if the patient is **unstable or develops tamponade**⁉️
🚨 **Urgent pericardiocentesis** is indicated
272
Why are **colchicine**, **glucocorticoids**, and **diuretics** **not first-line treatments** for **uremic pericarditis⁉️**
* ⛔ These are **used in non-uremic (idiopathic or viral) pericarditis**
* ➡️ They **do not address the uremic cause and do not remove toxins**
273
Why is the **renal outer medulla** particularly vulnerable in prerenal AKI⁉️
🔬 Due to its **limited blood supply** and **high metabolic demand,**
➡️ The **outer medulla** is **most susceptible to ischemic injury**
274
When is **renal biopsy** indicated in the evaluation of kidney disease⁉️
🔬 Only indicated for:
1. ✅ **Nephrotic-range proteinuria**
2. ✅ **Unexplained glomerular disease suspicion**
* ⛔ Not routinely used for AKI with clear prerenal cause
275
What is the **general prognosis** for patients with **AKI** **due to hypovolemia** ⁉️
✅ **>80% recover completely** **with appropriate management**
✅ **Most do not require dialysis or biopsy**
276
Why is **hyperkalemia a medical emergency** in AKI⁉️
* 🚨 Hyperkalemia is **arrhythmogenic**
* ✅ Can cause **fatal cardiac arrhythmias**
* ✅ Requires **prompt treatment**
277
What is the **first step** in managing **severe** **hyperkalemia** **with ECG changes**⁉️
A:
🚨 **IV calcium gluconate**
✅ **Stabilizes cardiac membranes**
✅ Indicated when:
* **K⁺ ≥ 6.5 mmol/L**
* Or **ECG changes** (e.g., **tall T waves, wide QRS, sine wave)**
278
What are the **key electrolyte abnormalities** in **pre-renal AKI** due to **dehydration**⁉️
A:
📈 **Hypernatremia**
📈 **Hyperkalemia**
➡️ Result from **volume depletion and impaired renal clearance**
279
**After cardiac stabilization** in hyperkalemia, how is **potassium lowered**⁉️
* 🧪 **Two-step strategy**:
1️⃣ **Shift K⁺ intracellularly**:
* IV insulin + dextrose
* ± β2-agonists (e.g., albuterol)
2️⃣ **Remove K⁺ from the body:**
* Diuretics (if kidneys working)
* Hemodialysis (if severe AKI)
* GI binders (e.g., Kayexalate)
280
What are the **main indications** for **urgent treatment of hyperkalemia**⁉️
A:
🚨 Treat immediately if:
✅ **K⁺ > 6.5 mmol/L**
✅ **ECG changes** (e.g., peaked T waves, wide QRS)
281
What are the **ECG changes** associated with **severe hyperkalemia**⁉️
A:
📉 Hyperkalemic ECG findings:
✅ **Tall, peaked T waves**
✅ **Loss of P waves**
✅ **Widened QRS**
✅ **Sine wave pattern** (pre-terminal)
282
What are common causes of **hyperkalemia due to impaired excretion and cellular shift⁉️ paralysis**
📌 **Impaired excretion:**
✅ RAAS inhibition (ACEi, ARB, spironolactone)
✅ Tubulointerstitial disease
✅ Acute/chronic kidney disease
✅ Addison’s disease
📌 **Cellular shift:**
✅ Acidosis
✅ β-blockers, digoxin
✅ Rhabdomyolysis
✅ Tumor lysis
✅ Hyperkalemic periodic
283
What is **pseudohyperkalemia** and what causes it⁉️
🔬 Pseudohyperkalemia = **falsely elevated serum K⁺** due to:
✅ **Leukocytosis**
✅ **Thrombocytosis**
✅ **Erythrocytosis**
✅ **In vitro hemolysis**
284
What is the most likely **cause** of **AKI** in a patient with **fever**, **sore throat**, **hypotension**, **dry mucosa**, and** dark urine**⁉️
* 🧠 **Prerenal azotemia** **due to dehydration**
✅ Triggered by *fluid loss* (e.g. fever, vomiting)
✅ **Dark urine = concentrated urine, not blood**
285
What is **hypokalemic nephropathy** and what **causes it**⁉️
🧬 Hypokalemic nephropathy = **kidney damage due to prolonged severe hypokalemia**
✅ Causes include:
* **Chronic laxative abuse**
* **Diuretic use**
* **Primary aldosteronism**
286
What is the **pathologic renal effect** of **prolonged hypokalemia**⁉️
🔬 Causes **vacuolar degeneration** of proximal and distal tubular cells
➡️ Initially **reversible**, but chronic hypokalemia can lead to **irreversible CKD**
287
What is the **mainstay of treatment** in **hypokalemic nephropathy**⁉️
**💊 Correct the hypokalemia**
✅ Replenish potassium
✅ Address underlying cause (e.g., stop laxatives/diuretics)
288
❓What are key distinguishing **features of PSGN vs prerenal AKI**⁉️
* 📊 **PSGN**:
* RBC casts, hematuria
* **↓ C3**, normal C4
* Edema, HTN
* 📊 **Prerenal AKI**:
* No RBC casts
* High urine osmolality, low FENa
* Dry mucosa, hypotension
289
Why does **hyperlipidemia** occur in **nephrotic syndrome**⁉️
🧬 **Hypoalbuminemia** stimulates **hepatic synthesis of proteins**
➡️ Leads to **increased lipoprotein** production
📈 Results in **hypercholesterolemia and hypertriglyceridemia**
290
Why should **lipid-lowering therapy** be included in **nephrotic syndrome management**⁉️
💊 To **reduce risk of cardiovascular morbidity**
✅ Patients with nephrotic syndrome are **at high risk of atherosclerosis**
290
Which **glomerular diseases** typically **do NOT** present **with hyperlipidemia**⁉️
⛔ **Nephritic syndromes** (e.g., post-streptococcal GN, rapidly progressive GN, lupus nephritis)
➡️ Are not typically associated with **hyperlipidemia**
