Renal Flashcards
1
Q
Loop Diuretics
A
furosemide, bumetanide, torsemide
- inhibits water, Na, K, Cl transport
- inhibits Ca and Mg absorption across the thick ascending limb in the loop of henle
- causes dilute urine
- increased prostaglandin synthesis -→ improves renal blood flow
- Indication:
- HTN, edema (pulmonary, peripheral edema due to CHF, nephrotic syndrome, and cirrhosis), hypercalcemia, hypermagnesemia-→does not cause hyponatremia -→ loose more water than salt
- SEs:
- decreased electrolytes (hypoK, hypoCa, HypoMg, HypoCl)
- hyperglycemia, hyperuricemia (can precipitate gout)
- NSAIDs may decrease efficacy
- ContraIndicated in pt with sulfa allergy
2
Q
Thiazide Diuretics
A
- hydrochlorothiazide, chlorthalidone, chlorothiazide
- MOA: block NaCl reabsorption at the early distal convoluted tubule (diluting segment)
- leads to diuresis and inability to produce a dilute urine
- electrolyte imbalances caused by thiazide diuretics:
- hyponatremia
- hypokalemia
- hypercalcemia
3
Q
Net effect of increased calcitriol
A
aka Vitamin D
- increased absorption of calcium and phosphorous in gut
4
Q
Net Effect of Increased PTH
A
hypercalcemia, hypophosphatemia
5
Q
Net Effect of increased Calcitonin
A
hypocalcemia, hypophosphatemia
6
Q
Hypophosphatemia causes, s/sxs, txs
A
- Causes: renal losses-→ HyperPTH
- GI: severe malnutrition, malabsorption, alcoholism, phosphate binders
- S/sxs: Muscle weakness, bone pain, rickets, osteomalacia
- tx: mild or moderate: milk, sodium, or K-phosphate tablets
- SEVERE = <1mg/dL → IV phosphorus replacement
7
Q
Hyperphosphatemia causes and tx
A
- causes: CKD, AKI, hypoPTH, tissue breakdown: rhabdomyolysis, hemolysis, tumor lysis (these are problems that cause hypocalcemia as a result of hyper K)
- tx: management in CKD: low phosphorus diet, phosphate binders, dialysis
8
Q
Hypermagnesemia causes, sxs, and tx
A
- causes: in CKD, Mg containing antacids, enemas, epsom salts, magnesium citrate, milk of magnesia
- iatrogenic: pre-eclampsia
- Sxs: Mg = vasodilator
- levels > 4-6 mg/dL: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus
- levels > 8-12: flaccid paralysis, respiratory arrest, cardiac arrest
- Tx: Mild: d/c mg supplements
- severe: IV calcium (to protect heart), saline diuresis (to flush excess Mg), furosemide
- Dialysis
9
Q
Cisplatin
A
chemo drug
“punches holes” in renal tubules → hypoK and hypoMg
10
Q
Hypomagnesemia causes, s/sxs, treatments
A
- Causes: polyuria from osmotic diuresis, DKA, AKI, PPIs, diuretic use
- extracellular volume expansion: reduced Na and H20 reabsorption in PCT, so less passive Mg reabsorption
- Hypercalcemia = reduced Mg reabsorption
- Drugs: Cisplatin, aminoglycosides, amphotericin B
- S/sxs:
- cardiac: repolarization abnormalities, ventricular arrhythmias
- Neuromuscular: tremor, twitching, tetany, seizures, migraine
- ***can cause unexplained hypocalcemia (due to impaired PTH secretion) and hypokalemia (due to released inhibition of ROMK channel so increased distal K secretion***
- Tx:
-
Severe: Mg levels <1mg/dL
- 1-2 grams of Magnesium sulfate
- can cause diarrhea
- 1-2 grams of Magnesium sulfate
-
minimal or no sxs:
- oral repletion (diarrhea side effect)
- preferred: sustained release Magnesium chloride
- oral repletion (diarrhea side effect)
- Amiloride = prevents Mg wasting
-
Severe: Mg levels <1mg/dL
11
Q
Amiloride
A
prevents Mg wasting
reduces renal Mg excretion by increasing its reabsorption in the distal nephron
Mg repletion in CKD or AKI = half dosage with close monitoring
12
Q
Causes of Pre-Renal Acute Renal Failure
A
- due to volume loss, heart failure, or loss of peripheral vascular resistance → all lead to loss of perfusion in kidneys
- NSAIDs also can cause this (vasoconstriction of the afferent arteriole)
- ACEI and ARB block effect of angiotensin (vasodilation of the efferent arteriole)
- Diuretics
- ***Kidneys are working fine, the organs that perfuse the kidneys arent working properly***
13
Q
PreRenal Acute Renal Failure S/sxs, Dx, and Tx
A
- S/sx: weak oliguria (decreased urine output), dizziness, sunken eyes, tachycardia, orthostatic BP changes
- Dx: BUN:Cr > 20:1, urine osmolality > 500, FeNa <1%, FeUrea <35%, Urine Na <20 mEq/L
- Tx: tx with fluids, cardiac support, and/or tx shock
14
Q
RIFLE criteria and AKI
A
- Risk:
- GFR: increased SCr x 1.5 or GFR decrease greater than 25%
- UO (urine output): <0.5 ml/kg/h x 6 hours
- Injury:
- GFR: increased SCr x 2 or GFR decrease greater than 50%
- UO: < 0.5mL/kg/h x 12 hours
- Failure:
- GFR: increased SCr X 3, GFR decrease by 75%
- OR SCR >4mg/dL
- UO: < 0.3mL/kg/h x 24 hours or anuria x 12 hours
- GFR: increased SCr X 3, GFR decrease by 75%
- LOSS: persistent AKI = complete loss of kidney function > 4 weeks
- ESKD: greater than 3 months
15
Q
AKIN Classification/Staging Classification & AKI
A
-
Stage 1: Absolute SCr: ≥ 0.3mg/dL
- % SCr: 150-200% (1.5-2x)
- UO: <0.5mL/kg/hr x 6 hours
- → no need for renal replacement therapy
-
Stage 2: % SCr: 200-300% (2-3x)
- UO: <0.5mL/kg/hour x 12+ hours
- → no need for renal replacement therapy
-
Stage 3: Absolute SCr: ≥ 4mg/dL with an acute increase of at least 0.5mg/dL
- %SCr: 300% + (≥ 3x)
- UO: <0.3mL/kg/hr x 24 hours or anuria x 12 hours
- → need for renal replacement therapy indicates stage 3 regardless of serum creatinine or UO
16
Q
PostRenal AKI Etiology, S/sxs, dx, tx
A
- Etiology: obstruction (most common = prostate), bilateral outlet obstruction or bilateral ureteral obstruction
- S/sxs: oliguria or anuria +/- suprapubic pain
-
Dx: foley catheter placement to find source of obstruction
- if large urine output after foley = bladder, urethra, BPH
- if low urine output after foley = ureter obstruction or pathology
- Renal U/S but CT is most specific!!
- tx: removal of obstruction → if done rapidly = quick reversal of AKI
17
Q
Acute Tubular Necrosis Etiology
A
- ***Type of Intrinsic AKI***
- Etiology = kidney ischemia or toxins
- prolonged pre-renal AKI = most common cause
-
Major Causes:
- drugs and toxins: ampho B, cisplatin, sulfa drug, aminoglycosides, radiocontrast media, NSAIDs, ACEI, cocaine use
- ischemic related ATN : dehydration, shock, sepsis, hypotension
- endogenous toxins: heme from hemolysis, myoglobin from rhabdomyolysis (iron is myoglobin is toxic to renal epithelial cells), tumor lysis syndrome, muscle breakdown in a marathon runner
18
Q
Acute Tubular Necrosis S/sxs, Dx, Tx
A
- S/sxs: Oliguria, increased SCr etc
-
Dx: urinalysis = muddy brown casts (renal tubule epithelial cells), myoglobinuria, hemoglobinuria
- FeNa >2%, FeUrea >35%, Urine Osmolality <350
-
Tx: remove toxin or re-perfuse kidney via IV fluids
- can use loop diuretics if pt is euvolemic and not urinating
- ***most pts return to baseline within 7-21 days ***
19
Q
Etiology of Interstitial Nephritis
A
- Etiology: immune-related response
- due to:
- drugs: PCN, sulfa (bactrim), NSAIDs, phenytoin, Diuretics, etc
- immunologic & infx disease: strep (get an ASO antibody), SLE, CMV, Sjogren’s, sarcoidosis
20
Q
Interstitial Nephritis S/sxs, Dx, & Tx
A
- ***type of intrinsic AKI***
- S/sxs: oliguria, increased SCr
-
Dx: urinalysis = WBC cats, WBCs, and eosinophils
- acute azotemia (accumulation of nitrogenous waste, BUN)
- diagnosed with RENAL BIOPSY → interstitial inflammatory cell infiltrates
-
Tx: d/c offending drug, corticosteroids, dialysis PRN
- → usually self-limiting if caught early
- most people recover kidney function within 1 year
21
Q
Etiology of Nephrotic Syndrome
A
- glomerular damage results in higher loss of proteins in the urine
-
Most common primary causes:
- membranous nephropathy: most common in non-DM adults associated with malignancy
- MINIMAL CHANGE DISEASE: most common cause in children, idiopathic nephrotic syndrome sxs improve after tx
- focal segmental glomerulosclerosis: obese pts, heroin, and HIV (+) black males
-
Most common Secondary Cause:
- lupus
- DM
22
Q
Nephrotic Syndrome S/sxs, Dx, & Tx
A
- S/sxs: peripheral or periorbital edema, ascites, weight gain, fatigue, and HTN, frothy urine
-
Dx: serologic testing and renal biopsy
- proteinuria >3.5g/day = diagnostic ( 24h urine collection)
- urinalysis: free lipid or oval fat bodies or fatty casts → lipiduria
- Hypoalbuminemia < 3.5g/dL
- hyperlipidemia LDL > 130mg/dL, Triglycerides > 150mg.dL
-
Tx:
- tx the causative disorder, corticosteroids
23
Q
Etiology of Glomerulonephritis
A
- inflammation of the glomeruli due to blockage from immune complexes → immune response causes this
- Post-Infectious Group A strep → diagnosed with ASO titers and low serum complement
-
IgA Nephropathy (berger disease): Most common cause of acute glomerulonephritis
- young males after URI or GI infx (within 24-48 hours) → IgA immune complexes are first line defense in respiratory/GI secretions so infx → overproduction which damages the kidneys
- more common in asian population
-
Membranoproliferative Glomerulonephritis: caused by SLE, viral hepatitis (Hep C)
- secondary to immune-complex deposition or complement mediated mechanism
24
Q
Glomerulonephritis S/sxs, Dx, & Tx
A
- S/sxs: edema + HTN + hematuria + RBC casts, jaundice, HTN
-
Dx: urinalysis = hematuria >3 RBCs/HPF + RBC casts + proteinuria (1-3.5g/day)
- ASO titer for post-strep
- serum complement = decreased (not always
- RENAL BIOPSY = GOLD STANDARD
-
Tx: steroids and immunosuppressive drugs to control inflammation due to immune response
- dietary management = salt and fluid restrictions
- Dialysis if symptomatic azotemia
- ACEI/ARBs (enalapril or losartan) are renoprotective → BP goal <130/80
- use meds to control hyperkalemia
25
Q
Staging of CKD
A
Chronic Kidney Disease
- Stage 1: Normal GFR ≥ 90mL/min/1.73m2
- either persistent albuminuria or known structural or hereditary renal disease
- Stage 2: Mild GFR 60-89 mL/min/1.73m2
- Stage 3: Moderate GFR 30-59 mL/min/1.73m2
- Stage 4: Severe GFR 15-29 mL/min/1.73m2
- Stage 5: Kidney Failure GFR < 15mL/min/1.73
26
Q
Definition of CKD
A
dx: GFR < 60mL/min/1.73m2 for 3 months or any of the following:
- albuminuria: urine albumin: creatinine ratio >30mg/day
- proteinuria: urine protein: creatinine ratio > 0.2
- hematuria
- structural renal abnormalities ( solitary kidney, hx of abnormal renal histology hx of renal transplant)
27
Q
Etiology of CKD
A
- Diabetes = MOST COMMON CAUSE (30%)
- HTN (25%)
- chronic glomerulonephritis (15%)
- interstitial nephritis, polycystic kidney disease, obstructive uropathy
28
Q
S/sxs of CKD
A
- Pruritus = common, but difficult to tx
- Cardio: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis
- GI: (usually due to uremia) nausea, vomiting, loss of appetite
- Neuro: lethargy, confusion, tetany → (due to hypocalcemia), uremic seizures, peripheral neuropathy
-
Heme: normocytic, normochromic anemia (secondary to deficiency of erythropoietin)
- bleeding secondary to platelet dysfunction→ platelets do not degranulate in uremic environment
-
Endo/Metabolic:
- Ca2+/Phosphorus disturbances→ decreased renal secretion of phosphate leads to hyperphosphatemia → decreased production of 1,25-dihydroxy vitamin D → hypocalcemia → hyperparathyroidism
- hyperkalemia → decreased secretion and acidosis
-
Fluid & Electrolyte problems:
- volume overload: watch for pulm edema
- hyperkalemia: due to decreased urinary secretion
- hypermagnesemia: secondary to reduced urine secretion
- hyperphosphatemia: decreased clearance of phosphate
- metabolic acidosis: due to loss of renal mass (& therefore decreased ammonia production) & kidneys’ inability to secrete H+
29
Q
Dx of CKD
A
- Dx: GOLD STANDARD = GFR
- urinalysis: waxy casts, or granular casts → show dilation and hypertrophy of remaining nephrons
- Proteinuria
- elevated BUN & creatinine
- hyperphosphatemia & hypocalcemia
- low erythropoietin levels (due to loss of renal function)
- Tests to order: CBC, chem panel (CMP), iron studies, lipid profile, urinalysis
30
Q
Tx of CKD
A
- Tx: ACEI and ARBs → slow progression of renal dysfunction
- manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation
- Maintain HGB at 11-12 g/dl → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality
- Dietary management: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus
- Need for hemodialysis or kidney transplant
- PCV-23
- Fluid overload management: dietary salt <2 gm/day
- GFR > 30 → thiazide diuretics (hydrochlorothiazide, chlorthalidone)
- GFR <30 → loop diuretics (furosemide, torsemide, bumetanide)
- can use phosphorus binders to reduce hyperPTH → calcium carbonate, calcium acetate, sevelamer, lanthanum, iron
- tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level >22
31
Q
Renal Osteodystrophy
A
caused by secondary hyperPTH often as a result of CKD
- increased phosphate due to decrease in secretion in kidneys → decreases production of 1,25-dihydroxy vitamin D (Calcitriol) → hypocalcemia → hyperparathyroidism
- body then break down bones to increase serum calcium
32
Q
Hydronephrosis
A
- Urinary Tract obstruction that leads to the collecting system in one or both kidneys to dilate
- Etiology: kidney stones (uretral), tumors, bladder outlet obstruction (BPH or prostate cancer) and sloughed off renal papillae
-
S/sxs:
- usually asymptomatic
- can have change in urine output (Difficulty urinating/hesitancy), HTN, hematuria, and CVA tenderness, pain in the side, abdomen, or groin
- usually asymptomatic
-
Dx:
- UA→often benign but may show hematuria or elevated pH
- may have a palpable abdominal or flank mass caused by an enlarged kidney
- Labs: may have increased serum creatinine
- U/S: initial imaging that you should do → will show dilation of the collecting system in one or both kidneys
- CT Scan: indicated for those with flank pain and suspected nephrolithiasis or in pts whom visualization of the ureters is needed
-
Tx:
- Removal of obstruction → rapidly reversible if removed quickly, can lead to UTIs and possible ESRD
33
Q
Polycystic Kidney Disease
A
Autosomal Dominant → mutations of PKD1 or PKD2 → causes 10% of ESRD
- formation & enlargement of kidney cysts (cysts also common in the liver (most common), then spleen and pancreas
-
Pathophys:
- vasopressin (ADH) stimulates cytogenesis and eventually leads to ESRD over time
-
S/sxs: renal → abdominal pain & flank pain, nephrolithiasis, UTI and hematuria
- ~10% of pts have brain aneurysms (so be concerned about headache complains)
- abdominal fullness
- mitral valve prolapse and L ventricular hypertrophy
-
Dx: U/S → shows fluid filled cysts, CT scan will show large renal size and thin walled cysts
- need to U/s rest of direct family members
-
Tx: no cure, only supportive to ease sxs
- control HTN <130/80 with use of ACE-I & ARBs
- infx should be treated quickly/vigorously with abx
- dialysis or transplant should be considered when renal insufficiency becomes life threatening
34
Q
Renal Vascular Disease
A
aka renovascular HTN
- HTN caused by renal artery stenosis in one or both kidneys
- ***MOST COMMON cause of secondary HTN***
- Pathophys: decreased renal blood flow leads to activation of RAAS
- Etiologies: atherosclerosis = most common in elderly, fibromuscular dysplasia = most common cause in women <50
-
S/sxs:
- suspect in pts with headache & HTN <20 years
- or >50 years, severe HTN or HTN resistant to 3+ drugs
- or abdominal bruits
- or it pt develops AKI after the initiation of ACE-I therapy
-
Dx:
- non-invasive option: CT angiography, MR angiography, Duplex doppler (duplex doppler = less sensitive, specific)
- Renal Catheter Arteriography = GOLD STANDARD and definitive → revascularization can be performed during the same procedure if stenosis is found (not used in pts with renal failure)
-
Tx:
- Revascularization = definitive management
- angioplasty with stent → performed if creatinine >4.0, increased creatinine with ACE-I tx, or >80% renal stenosis
- Bypass if angioplasty is not successful
- Medical Management:
- ACE-I or ARBs (BUT these are contraindicated in pts with bilateral stenosis or solitary kidney b/c can cause AKI due to ischemia
35
Q
ESRD, Etiology, Dx, and Tx (NOT S/Sxs)
A
End Stage Renal Disease
- Stage 5 CKD → GFR <15, complete loss of kidney function for more than 3 months
- Most Common Cause = DM
-
Dx:
- GFR <15mL/min/1.73m2 for ≥3months
- low EPO levels
- metabolic acidosis
- increased potassium, phosphate, and PTH
- low calcium, sodium, bicarb
- “Waxy” cats with low urine flow
-
Tx:
- Dialysis & kidney transplant
- Manage co-morbidities:
- bring HGB up to 11-12 (no higher or else possibility of clots)
- dietary management: protein restrictiion, Calcium and Vitamin D supplements, limit water, sodium, potassium, and phosphorus
- ACE-I & ARBs = slow progression of renal dysfunction
- Loop diuretics: preferred addition to the management of edema associated with HTN due to ESRD
- Pneumococcal vaccine
36
Q
S/sxs of ESRD
A
End stage renal disease
-
S/sxs:
- pruritus
- HTN, may have A/B nicking, copper wire changes on retina
- S4 heart sound
- Kidneys affected by ESRD cannot regulate levels of electrolytes → sodium excess = retention of water
- potassium excess = abnormal heart rhythm, can lead to cardiac arrest
- magnesium deficit = can affect heartbeat and cause changes in mental state
-
Hormones: cannot absorb calcium and bones become weak and may break (renal osteodystrophy)
- erythropoietin production decrease = normochromic, normocytic anemia
- Enzymes: kidneys affected by ESRD respond to lower GFR by making too much renin → keeps blood pressure levels high → difficult to tx
37
Q
Hyperkalemia and EKGs
A
- shortened QT
- ST depression
- Peaked T wave
38
Q
Hypokalemia and EKGs
A
- decreased T-wave amplitude
- ST depression
- increased U-wave amplitude
39
Q
Hypokalemia Causes
A
-
Urine potassium < 20mmol/L
- metabolic acidosis: diarrhea, laxative
-
Urine potassium > 20 mmol/L
-
metabolic acidosis:
- proximal RTA, or distal RTA
-
Metabolic Alkalosis + Normal or Low BP
- Low urine chloride (<20)
- vomiting
- High Urine Chloride (>20)
- Lasix
- thiazide
- Mg depletion
- Bartter’s
- Gitelman’s
- Low urine chloride (<20)
-
Metabolic Alkalosis + High BP
- increased renin + increased aldosterone:
- renal artery stenosis or renal tumors
- decreased renin + increased aldosterone
- primary aldosteronism
- decreased renin + decreased aldosterone
- Cushings
- liddles
- apparent mineralocorticoid excess (licorice, drugs)
- MR mutation
- increased renin + increased aldosterone:
-
metabolic acidosis:
51
Q
Hypervolemic Hyponatremia
A
Hypotonic hyponatremia (osmolarity <275 mOsm/L)
- body gains excess Na+ and Water
- but Water >>>>>Na+
- Causes: HF, cirrhosis, nephrotic syndrome
- tx: Fluid & Na+ restriction (i.e. 2 gm/day)
- optimize the underlying disease state
- diuretics
- increase the intravascular oncotic pressure (albumin)
- pulls fluid of out intracellular compartment
52
Q
Euvolemic Hyponatremia
A
aka isovolemic hyponatremia
hypotonic hyponatremia (osmolarity <275 mOsm/L)
ECF volume is normal
-
have excess water → total body water >>>>normal total Na+
- water intoxication
- causes: SiADH (too much ADH secreted), Polydipsia, decreased water secretion
- carcinomas (small cell lung cancer)
- CNS disorders → stroke, meningitis, trauma
- medications: SSRIs, NSAIDs, antipsychotics, sulfonylureas
- Tx:
-
Non-acute (Na >115mEq/L and asymptomatic:
- fluid restriction, possible chronic therapy
-
Acute (Na <115 mEq/L and/or sxs):
-
3% NaCl infusion
- +/- diuretics to correct fluid accumulations
- fluid restriction → 1000-1200mL/day
-
3% NaCl infusion
- ******no more than 12 mEq/L/24 hours (0.5mEq/hour)******
- can cause osmotic demyelination syndrome → myelin cells swell/shrink and die
-
Non-acute (Na >115mEq/L and asymptomatic:
53
Q
Hypovolemic Hyponatremia
A
hypotonic hyponatremia (osmolarity <275 mOsm/L)
decreased ECF volume
- decrease in both Na+ and Water
- deficit of Na+ >>>>> deficit of water
- Causes:
- diuretics (thiazides), diarrhea, vomiting, NG suction
- Treatment: NS @ 300ml/hr until improvement in symptoms
- *****DO NOT CORRECT SODIUM LEVELS >12mEQ/L/24 HOURS******
56
Q
Hypovolemic Hypernatremia
A
- when water loss >>>sodium loss
- causes: diarrhea, sweating, diuretics
- tx: d/c diuretics or laxatives
-
if symptomatic: initially 200-300ml/hr with NS (to achieve hemodynamic stability)
- replace free water deficit: D5W, ½ NS or a combo
- asymptomatic: D52, ½ NS, or a combo
-
if symptomatic: initially 200-300ml/hr with NS (to achieve hemodynamic stability)
57
Q
Isovolemic Hypernatremia
A
aka euvolemic hypernatremia
water loss only
- causes:
-
Diabetes insipidus:
- central DI = decreased ADH production
- Nephrogenic DI = decreased renal response to ADH
- drug induced DI:
- aminoglycosides, Ampho B, cochicine, demeclocycline (used to tx chronic euvolemic hyponatremia)
-
Diabetes insipidus:
- Tx:
- initially: D5W (replace free water)
-
chronically:
- for central DI: desmopressin (DDVAP) b/c it is a synthetic analog to ADH → act on the V2-receptors of collecting duct → water reabsorption
- for nephrogenic DI: NSAIDs [can cause euvolemic hyponatremia] (indomethacin, IBU, naproxen, diclofenac, ketoprofen) and thiazides
60
Q
Hypervolemic Hypernatremia
A
body has excess sodium and water
sodium >>>> water
- causes:
- renal failure
- Tx:
- replace intravascular deficit if necessary (use D5W, ½ NS or a combo)
- loop diuretics (if making urine) (increases sodium excretion)
- hemodialysis
