MF2 RENAL Flashcards

(50 cards)

1
Q

Which kidney is higher

A

left

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2
Q

Describe the vasculature of the kidney

A

renal artery → segmental arteries → interlobar artery → arcuate artery → cortical radiate arteries → afferent arterioles → glomerular capillaries → efferent arterioles → peritubular capillaries and/or vasa recta → interlobar veins → arcuate veins → interlobar veins → segmental veins → renal vein

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3
Q

Risk factors of upper UTI

A
  • Female
  • Sexual intercourse
  • Indwelling catheter
  • Diabetes mellitus
  • Urinary tract obstruction
  • Vesicoureteral reflux: primary congenital defect, bladder outlet obstruction)
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4
Q

Risk factors of lower UTI

A
  • Sexual intercourse
  • Female
  • Post-menopause (decreased estrogen)
  • Foley catheter
  • Hyperglycemia
  • Impaired bladder emptying
  • Poor hygiene
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5
Q

Symptoms and Urinalysis for UTIs

A

SYMPTOMS
- Lower
> Dysuria
> Increased frequency
> Increased urgency
> Suprapubic pain
- Upper
> Fever
> Chills
> Flank pain (costovertebral engle)
- Kids
> Delirium
> Fatigue
> Incontinence
- Elderly
> Irritable
> Malodorous
> Fever even in lower

URINALYSIS
- WBCs
- Leukocyte esterase
- Nitrates
- Hematuria

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6
Q

Radiology for UTI diagnoses

A
  • Renal ultrasound: can be used with kids with kidney malformation that can lead to UTI
  • Bladder Ultrasound
  • Voiding (VCUG) cystourethrogram: radiocontrast on fluoroscopy to watch urination
    > Vesicoureteral reflux
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7
Q

Types of Kidney Stones

A

Nephrolithiasis: solutes in urine precipitate out and crytallize

  • Calcium stones: calcium oxalate (80%) or phosphate
  • Uric acid: lose too much fluid, high protein diet, diabetes, metabolic syndrome
  • Struvite: magnesium ammonium phosphate → upper UTI
  • Cysteine stones: rare disorder → cystinuria

Xanthogranulomatous peylonephritis: infected kidney stone causes chronic obstruction → infection and increased pressure

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8
Q

Kidney stones treatment

A
  • Shockwave lithotripsy
  • Medications
    > a-blockers/CCB
    > NSAIDs/opiates
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9
Q

Receptors in bladder and urethra

A
  • B3 on bladder wall: binds NE; relax bladder
  • M3 on bladder wall: binds acetylcholine; contract detrusor
  • Stretch receptors on bladder wall: detect rugae expansion
  • a1 on internal sphincter: binds NE; closes sphincter
  • N1 on external sphincter: binds Ach; closes sphincter
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10
Q

Nephrotic syndrome (subtypes, causes)

A

Massive proteinuria, hypoalbuminemia, hyperlipidemia, edema

  • Increased permeability through damaged glomerular basement membrane
  • PRIMARY (intrinsic kidney disease)
    > Membranous glomerulonephritis: white adults,
    thickened basement membrane from auto-Abs
    - HBV, SLE, solid tumors (lung, breast, GI)
    > Minimal change glomerulonephritis: children; if adult
    check hematological malignancy;
    - NSAIDs
    ***PERIORBITAL EDEMA IN KIDS
    > Focal segmental glomerulosclerosis:
    - African ancestry, obese, HIV, scaring/sclerosis of
    glomerulus
  • SECONDARY (systemic disease, congenital)
    > Nodular Glomerulosclerosis
    - DM: hyperglycemia → glycation → thickened
    basement membrane → hypertrophy, scarring,
    thickening
    - Amyloidosis: nodular deposits
    > Focal segmental glomerulosclerosis: podocytes
    - Inherited, heroin
    > Membranoproliferative GN
    - HCV, malaria, SLE, leukemia, lymphoma, shunt
    neprhitis
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11
Q

Factors affecting GFR

A
  • Pressure out
    > Glomerular hydrostatic pressure: out capillaries
  • Pressure in
    > Colloid pressure: by plasma proteins pulling water
    > Scapular hydrostatic pressure: fluid backup
  • KF
    > Surface area of glomeruli
    > Permeability of glomeruli
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12
Q

Diagnosing Nephrotic syndrome

A
  • Urinalysis
    > 3+ or 4+ proteinuria (dipstick)
  • Blood test
    > Hypoalbuminuria
    > Hyperlipidemia
    > HIV, Hep C (FSG)
    > Autoantibodies (membranous)
    > Cancer
  • Physical exam
    > Edema
  • Renal biopsy
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13
Q

Nephrotic syndrome treatment

A
  • Corticosteroids: immune suppression
    > Prednisone
  • Diuretics: loo diuretics for edema
    > Furosemide
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14
Q

Nephron - Proximal Convoluted Tubule

A
  • 3NA/2K pump, water follows
  • NaCl channel
  • Amino acids
  • SGLT2 transporter (glucose)
    > Jiardiance is an inhibitor; used for diabetes, HTN
  • HCO3 reabsorb, Na & H antiporter
    > Acetazolamide inhibits → Na/H2O excretion, acidosis
    > Impaired = type II renal tubular acidosis
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15
Q

Nephron - Loop Henle

A
  • Aquaporin I: water pump
    > Mannitol increases gradient → more reabsorption
  • Na/K/2Cl cotransporter
    > Loop diuretics inhibit (furosemide)
    > Barters type I syndrome
  • ROMK: K pump
    > Barter’s type III
  • IC-KB: Cl pump
    > Barter’s type II
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16
Q

Nephron - Distal Convoluted Tubule

A
  • NaCl pump
    > Thiazide diuretics inhibit (increased Ca absorb)
    > Gitleman’s syndrome
  • 3Na/2K pump, water follows
  • Ca channel
    > Hypercalcemia: cancer if admitted, hyperparathyroidism
    if outpatient
    > PTH activates this channel
  • Na pump
    > Aldosterone activates (activated by ACE)
  • K pump
    > Aldosterone activates (activated by ACE)
    -3Na/2K pump, water follows
    > Aldosterone activates (activated by ACE)

**K sparing diuretics inhibit aldosterone (receptor agonist)
> Spironolactone
**Type IV renal tubular acidosis inhibits aldosterone

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17
Q

Nephron - Collecting system

A
  • Intercalated A cells: secrete H
    > Inhibition is type IV renal tubular acidosis
  • Intercalated A cells: reabsorb H
  • Aquaporin II: pump water
    > Activated by ADH (activated by increased plasma
    osmolarity, decreased blood volume)
    > Activated in SIADH (urine concentrated, euvolemic; small
    cell lung cancer)
    > Inhibited by chronic lithium (bipolar meds, diabetes
    insipidus; urine dilute, inappropriate)
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18
Q

Barter’s Syndrome

A
  • Loop of Henle issue → acts like loop diuretic
  • Infants
  • Increased renin
  • Increased aldosterone
  • Decreased Na, K, Cl
  • Increased HCO3 → alkalosis
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19
Q

Gitleman’s sydrome

A
  • NaCl pump issue in DCT → acts like thiazide diuretic
  • Teenage
  • Alkalosis
  • Hypokalemia
  • Decreased Mg
  • Often asymptomatic; muscle weakness, fatigue, dizziness, vertigo, plyuria, nocturia
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20
Q

Hypernatremia and Hyponatremia

A

**Disorders of water balance

HYPERNATREMIA
- Decreased volume
> Dehydrated (less urination) or diabetes insipidus
(increased urination)
- Increased volume
> Excessive IV or hyperaldosteroneisma
- SYMPTOMS: tired, weak, altered mental status, seizures
***cerebral edema

HYPONATREMIA
- Hyperosmolar
> Hyperglycemia
- Iso-osmolar
> Lab error
> Multiple myeloma
- Hypo-osmolar
> Hypervolemic: CHF, cirrhosis, nephrotic syndrome
> Euvolemic: SIADH, Addison’s, hypothyroid, adrenal
insufficiency
> Hypovolemic: renal or GI fluid loss
- SYMPTOMS: neurological predominate (headache, nausea, malaise, lethargy, weakness, muscle cramps, anorexia, disorientation)
***cerebral demyelenation syndrome (“locked in”)

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21
Q

Hyperkalemia vs Hypokalemia

A

HYPERKALEMIA
- Increased intake
> IV
- Transcellular shift
> Cell injury
> Metabolic acidosis
> Tumor lysis
- Decreased loss
> Decreased GFR, hypoaldosterone
- SYMPTOMS: muscle weakness, arrhythmias, paralysis, nausea, palpitations, muscle stiffness
> ECG changes and cardiotoxicity (peaked & narrow T, loss
P, long PR, wide QRS, AV block)

HYPOKALEMIA
- SYMPTOMS: usually asymptomatic; muscle cramps, arrhythmias, fatigue, myalgia, constipation
- Decreased intake
> Anorexia
> Alcoholism
- Transcellular shift
> Alkalemia, insulin, hyperaldosterone
- Increased loss
> Renal: loop diuretics/Bartter’s, thiazide/Gittleman’s
> GI: vomiting (increase pH), diarrhea (decrease pH)

22
Q

Hypertension

A

ESSENTIAL (95%)
- Increased sympathetic NS activity
> Obesity (high catecholamines)
> High stress (high cortisol)
- Increased renin release
> Diabetes
> Obesity
- Increased Na retention (“low renin HTN”)
> African American
- Increased age (decreased compliance, increased TPR)

SECONDARY (5%)
- Renal
> Vascular: fibromuscular dysplagia, renal artery stenosis
> Parenchyma: diabetic nephropathy, glomerulonephritis,
polycystic kidney disease
- Cardiac
> Coarctation of aorta (diff BPs upper vs lower)
- Lungs
> obstructive sleep apnea
- Neuro (ICP)
> Cushings triad: high BP, low HR, irregular respiration
- Drugs
> Sympathomimetics (cocaine, NMDA, PCP,
amphetamines, ADHD meds)
> Estrogen contraceptives (estrogen increased liver AII)
> NSAIDs (inhibit COX2 → constrict afferent → low GFR)
- Pregnancy
> Preeclampsia: >20wks, HTN, proteinuria
> Eclampsia: >20wks, HTN, proteinuria, seizures
- Endocrine
> Adrenal
- Cortisol → Cushing’s syndrome
- Aldosterone → hyperaldosterone → high Na → BV
- Norepinephrine → pheochromocytoma
> Thyroid
- Hypothyroid
- Hyperthyroid
- Hyperparathyroid → increased Ca → vasoconstriction

23
Q

HTN medications

A
  • ACEi: avoid in asthma, african american, pregnant, renal arterial sclerosis
  • ARBS
  • Dihydropiridine CCBs: good in low renin HTN
  • Thiazide diuretics
  • B-blockers: careful in COPD, asthma
  • Aldosterone antagonists (K sparing diuretics)
  • Alpha 1 blockers/ alpha 2
24
Q

HTN meds in pregnancy

A
  • Hydralizine: vasodilator
  • Methyl-dopa: alpha-2 agonist
  • Lavetalol: beta blocker
  • Nifidipine: Ca channel blocker
25
HTN emergency
- Decrease BP 25% in 2hr → <160 in 24hr → baseline in 2 days - IV medications: > Nicardipine * > Nitroprusside > Nitroglycerine > Esmolol (aortic dissection) > Labetalol *
26
Acidemia
---RESPIRATORY--- - Decreased resp rate → increased pCO2 > CNS depression > Neuromuscular > Obstructive lung disease **Compensation HCO3:pCO2: acute 1:10, chronic 3:10 ---METABOLIC--- **Compensation pCO2 = 1.5 x HCO3 + 8 - AGMA (>12) > Ketoacidosis > Uremia > Lactic acidosis (decreased O, decreased clearance [liver/renal failure], sepsis) > Toxins - Methanol - Ethylene glycol (antifreeze) - Propylene glycol - Salicylates (tylenol, aspirin) > Renal failure ***Delta ratio (AG/HCO3) > 0.4 - 0.8: AGMA + NAGMA > 1 - 2: pure AGMA > 2+ : Metabolic alk + AGMA > < 0.4: Hyperchloremic - NAGMA (<12) > Renal - Renal tubular acidosis (hypoK [type I, II], hyperK IV) - Renal Failure > Extrarenal - Saline infusion - TPN - Ureteral divergence - Pancreatic fistula - Addison's, acetazolamide - Diarrhea
27
Alkalemia
---RESPIRATORY--- - Increased resp rate > CNS hyperactivity > Hypoxia (penumonia, PE) **Compensation HCO3:pCO2: acute 2:10, chronic 4:10 ---METABOLIC--- - Decreased H > Vomiting > NG tube - Increased HCO3 > Total volume loss (shock, diuretics) > Mineralcorticoid excess (hyperaldosterone; Cushing's) > Over-reaction hypercapnia (COPD) **Compensation pCO2 = 1.5 x HCO3 + 8
28
Types of shock
Inadequate tissue perfusion → ischemia → necrosis → organ failure HYPOVOLEMIC - Decreased cardiac output, increased resistance, increased HR, cyanosis - Blood loss: GI bleed, AAA rupture, trauma, post-partum - Non-blood fluid loss: burns, vomit, diarrhea, bowel obstruction, DKA CARDIOGENIC - Decreased circulating volume → low BP → high HR → RAAS → ischemia → deacreased ATP & increased lactate → organ failure - MI, myocarditis, aortic/mitral valve stenosis, arrhythmias OBSTRUCTIVE - Tension pneumothorax - Pericardial tamponade - Pulmonary embolism - Proximal aortic dissection DISTRIBUTIVE - Septic shock > inflammation, acute phase reactant proteins, endotoxins decrease plasmin - Anaphylactic > Leukotrienes, histamines - Neurogenic > Acute spinal cord injury > Regional anesthesias
29
Normal saline vs Ringer's lactate
Normal: high Cl content → hypercloremia if long time Ringers: NaCl, CaCl, KCl; closer to body composition
30
Pre-renal AKI
Blood supply to kidney decreased BUN/cr > 20:1 Decreased GFR High blood Na and water FENa < 1% Less urea, Na, water in urine - Decreased blood volume > CHF > Liver failure > Kidney injury > Pancreatitis > Shock > Diarrhea > Vomitting > Burns - Large vessel block > Renal artery stenosis > Afib - Small vessel block > Hepatorenal syndrome: liver failure → portal hypertension → vasodilators compensation → low BP > NSAIDs > Increased Ca (vasoconstriction) > ACEi/ARBs: dilate efferent
31
Intrinsic AKI
Kidney cell damage BUN/cr < 15:1 Decreased GFR Low blood Na and water FENa > 2% High urea, Na, water in urine Proteinuria, hematuria - Acute tubular necrosis > Ischemia: decreased blood flow, rhabdomyolysis, sepsis, HF > Toxins: - Meds: NSAIDs, aminoglyosides, vancomycin, antiviral acyclovir, IV contrast dye - Hemolysis: Hb and Fe - Cancer: uric acid metabolism waste product - Multiple myeloma: bets jones proteins - Ethylene glycol: antifreeze **Rise in Cr, oligouric → diuretic → recovery, hyperK, metabolic acidosis - Glomerulonephritis > Podocytes: SLE, membranous glom, diabetes > Basement membrane: anit-GMB Abs (Good Pastors_ > Immune-complex mediated: post strep, endocarditis, Hep B, C, IgA nephropathy - Acute interstitial nephritis > Medications: B-lactams, PPIs, NSAIDs, sulfonamides > Sarcoidosis: granulomas deposited in tissues > Amyloidosis: B plaques deposited in tissues > Infection: systemic infection, direct renal infection > Lupus: auto-Abs
32
Post-renal AKI
Obstruction - Ureter > Kidney stones > Intra-abdominal tumor - Bladder > BPH > Prostate cancer > Uterine prolapse > Hypoactive bladder
33
Complications of AKI
- Uremia: > platelet dysfunction → bleeding > pericarditis → pericardial effusion → tamponade > excess neuron firing → seizures, encephalopathy, asterixis - Acidosis: > Injured tubules → arrhythmias, hypotension - Drugs: > Less excretion - Electrolytes: > Less K excretion → hyperK → arrhythmias > Hyperphosphatemia
34
Investigation of AKI
IS IT AKI? - Creatinine elevated - Decreased urine outpus WHAT IS THE CUASE - Pre-renal AKI > WBC casts, bacteria, nitrates on urinalysis → sepsis > Low Na and urea in urine & hypervolemic → CHF, hepatorenal syndrome, nephrotic syndrome > Low Na and urea in urine & hypovolemic → burns, dehydrates, vomiting, diarrhea - Intrinsic AKI > WBC casts, bacteria, nitrates on urinalysis → pyelonephritis > WBC casts, eosinophils → AIN > RBC casts, proteinuria, lipiduria → glomerulonephritis > Muddy brown casts → acute tubular necrosis > High Na and urea in urine - Post-renal AKI > Renal ultrasound, CT (+bladder scan) → hydronephrosis, tumors/masses - Other > Hx CKD, small atrophic kidneys on imaging
35
Indications for renal replacement therapy
- Acidosis: can't secrete H - Electrolytes: severe hyperK - Intoxication: high drug accumulation - Overload: severe volume overload - Uremia: encephalopathy, seizures
36
Causes of CKD
- HTN: hyperfiltration → cell necrosis → GLOMERULOSCLEROSIS → low GFR - Diabetic nephropathy: non-enzymatic glycation → inflammatory molecules → arteriosclerosis → higher pressure → GLOMERULOSCLEROSIS → low GFR - Glomerulonephritis: immune complexes on BM → infalmmation → hyperfiltration → high GFR → mesangial cells try to correct → TGF-B → GLOMERULOSCLEROSIS → low GFR - Polycystic kidney disease: cysts compress nearby vessles → low GFR → ischemia → necrosis → renin release → HTN → GLOMERULOSCLEROSIS - NSAIDs: PGI2 and PGE2 vasodilate afferent arterioles → high [NSAIDs] inhibit → vasoconstriction → low GFR - AKI: prolonged or frequent
37
Diagnosing CKD
- Kidney injury for 3+ months > GFR (normal 125 mL/min) - Stage 1: >90 - Stage 2: 60-89 - Stage 3a: 45-59 - Stage 3b: 30-49 - Stage 4: 15-29 - Stage 5: <15 > Creatinine - Albuminuria (urine albumin:cr) > Mild: <30 > Moderate: 30-299 > Severe: > 300 - Renal ultrasound > Polycystic > Small, atrophied kidneys > Vascularity - Renal biopsy and serology > ANA (SLE), RF (RA), HIV, Hep - Additional tests > BMP: hyperK, hyperPHOS, hypoCa, hypo/hyperNa > CBC: anemia > ABG: metabolic acidosis > Lipid panel > PTH levels: hyperparathyroidism, hyperCa in severe CKD
38
CKD complications
- Electrolytes > HyperK: less filtration K → arrhythmias > Low vitD: kidney enzymes make vitD → low Ca absorb > HyperPHOS: less vitD → low Ca → low PO4 excretion > Na fluctuates - Retention of fluid → delusional hyponatremia - Worse GFR → cannot excrete Na → hyperNa - Water imbalance > Low GFR → water retention → volume overload → edema → pulmonary, peripheral, HTN > Damage to kidney → albuminuria → edema - Waste removal > Urea build up: Azotemia → encephalopathy, seizures, fatigue, nausea, vomiting, uremic pericarditis, uremic frost, platelet interference (can't clot) - Hormone imbalance > Erythropoietin: kidney makes EPO > Renin: released with low GFR > PTH: low vitD → low Ca → PTH release → release bone Ca → renal osteodystrophy, osteitis cystica fibrosa - Metabolic acidosis: a-intercalated cells damaged - Albumin regulation: albuminuria → third spacing fluid → liver makes proteins → hyperlipidemia - Erectile dysfunction: HTN → atherosclerosis/ep damage → less blood flow
39
CKD treatment
- HTN: ACEi/ARBs (avoid ACEi in severe CKD) - Water retention: loop diuretics, Na/H2O restriction - Glomerulonephritis: steroids - HyperK: insulin, SABA, loop diuretic - HyperPHOS: sevelamer HCl - HypoCa: Ca, vitD - Anemia: synthetic EPO, IV iron - Low albumin: ACEi/ARBs - Hyperlipidemia: statinds - Platelet activity: DDAVP
40
PKD
Polycystic Kidney Disease - Cysts compress blood vessels → necrosis, low GFR → HTN - Cysts compress collecting → urinary stasis → stones - Flank pain, hematuria → eventual renal failure - Ca influx → cell proliferation → water pumps activated - Autosomal Dominant PKD > Adult; inherited PKD1/PKD2 mutation then random > PKD1 more severe > Cysts can pop up on liver, seminal vessels, pancreas, vasculature - Autosomal Recessive PKD > Infant > Prenatal ultrasound > Congenital hepatic fibrosis: portal hypertension > Ascending cholangitis: block bile ducts → cholestasis
41
Major functions of the kidney
1. Waste excretion: nitrogenous (urea, Cr), urate, drugs, peptide hormones 2. Electrolyte balance and osmoregulation: NaCl, K, H, HCO3, Ca, Mg, PO4 3. Hormonal synthesis: EPO (cortex), vitD activation (PCT), renin (JGs) 4. Blood pressure regulation: Na excretion, renin 5. Glucose homeostasis: gluconeogenesis (lactate, pyruvate, AAs), clearance of insulin
42
Glomerular basement membrane
1. Mesengial cells: support capillaries, contractile (can alter GFR), can secrete chemo/cytos, minimize accumulation 2. Capillary endothelial cells: fenestrated; interface with blood (target for antibodies and contact site for neutrophils/lymphocytes) 3. Visceral epithelium/podocytes: interdigitated foot processes (slit diaphragm) 4. Parietal epithelium: line interior of Bowman's capsule, contain podocyte progenitor population 5. Juxtaglomerular cells: smooth muscle lining afferent arteriole; renin
43
Factors affecting GFR
Afferent arteriole - Prostaglandins = dilation → increase GFR - NSAIDs = constriction → decrease GFR Efferent arteriole - ACEi = dilation → decrease GFR - Angiotensin II = constriction → increase GFR
44
GFR autoregulation
1. Myogenic mechanism: release vasoactive factor (prostaglandins, NO → increase GFR) 2. Tubuloglomerular feedback: changes in Na delivery to macula densa lead to changes in afferent arteriole tone (increased Na delivery → afferent constriction → decrease GFR)
45
RAAS System
Stimuli for renin release: > Decrease stretch of afferent arteriole > JG B-adrenergic receptor stimulation > Low Na in fluid composition at macula densa in DCT AII targets: > Vasocontriction > Increased vascular smooth muscle growth > Increased aldosterone → Na retention > Increased bicarbonate products
46
Urinalysis Dipstick
1. Specific gravity > Mass of equal volumes of urine/H20; 1.001-1.030 > If <1.010 = dilute, >1.020 = concentrated > 1.010 = isosthenuria (same specific gravity as plasma) 2. pH > 4.5-7.0 > Persistent alklaline → RTA, UTI 3. Glucose > Hyperglycemia, increased GFR, PCT dysfunction (Fanconi), SGLT2 inhibitors 4. Protein 5. Leukocyte esterase > Infection (UTI) or inflammation (AIN) along urinary tract 6. Nitrites > UTI 7. Ketones > Alcoholic/diabetic ketoacidosis 8. Hemoglobin > Hemolysis (hemoglobinuria), rhabdomyolysis (myogolobinuria), true hematuria
47
Urine microscopy (Cells, casts, crystals)
RBCs > Dysmorphic = glomerular bleeding (glomerulonephritis) > Isomorphic = bladder cancer Leukocytes > Inflammation > Infection Eosinophils > AIN > Atheroembolic disease (plaque from large arteries blocks renal arteries) Oval fat bodies (renal tubular cells filled with lipid) > Nephrotic syndrome Casts > Hyaline = physiologic → concentrated, fever, exercise > RBC = glomerular bleeding → proliferative GN, vasculitis > WBC = pyelonephritis, interstitial nephritis > Muddy brown = ATN, acute proliferative GN > Fatty = Nephrotic syndrome Crystals > Uric acid = acidic urine, tumor lysis syndrome > Calcium phosphate = alkaline urine > Calcium oxalate = hyperoxaluria, ethylene glycol poisoning, nephrolithiasis > Sulfer = sulfa antibiotics
48
Nephritic-Nephrotic Spectrum
NEPHROTIC - Focal segmental glomerulosclerosis - Membranous glomerulopathy - Minimal change INTERMEDIATE - Membranoproliferative GN - Focal proliferative GN > IgA nephropathy (Berger's; local inflammation) > Idiopathic membranoproliferative GN > Hep B, C > SLE > Cryoglobunemia (form of vasculitis; cryoglobins clump) NEPHRITIC - Diffuse proliferative GN - Crescentic GN (chronic immune-mediated, glomerular inflammation and injury)
49
NSAIDs in nephrology
- Decrease GFR by constricting the afferent arteriole > Sodium retention, water retention > Hypoaldosteronism - HyperK - HTN > Vasomotor AKI (renal ischemia) > Acute interstitial nephritis > Chronic interstitial nephritis > Acute tubular necrosis
50
Presentation of end stage renal disease
1. Volume overload 2. Electrolyte imbalances > HyperK > HyperPO4 > Hyper uric acid > HypoNa > HypoCa (low vitD) > HypoHCO3 3. Uremic syndrome > Asterixis > SOB, pleuritic chest pain > weight loss, amennohrea > Anorexia, nausea, vomiting > Pruritus, pallow, jaundice > Palpable bladder, hematuria > Muscle weakness, cramps