| Question | Answer |
| What is the definition of acute renal failure? | rapid rise in BUN or creatinine over hours or days |
| What is BUN derived from? | protein waste products |
| How does liver disease effect BUN levels? | falsely low |
| Why does creatinine clearance slightly overestimate GFR? | there is some tubular secretion of creatinine; it is not all freely filtered |
| What is the cause of renal failure in patients with cirrhosis (hepatorenal syndrome)? | 1. portal hypertension leads to splanchnic vasodilation
2. decreased volume is sensed by JG apparatus → activation of RAAS
3. renal vasoconstriction → decreased renal perfusion |
| Patient with drop in oxygen saturation when they sit up | orthodeoxia, characteristic of hepatopulmonary syndrome |
| How would creatinine be effected in a patient with a large renal stone obstructing a ureter? | creatinine does not rise if there is a loss of only one kidney |
| How is postrenal azotemia diagnosed? | finding bladder distention or examination, bilateral hydronephrosis, or large volumes or urine after passing Foley |
| What is the most common cause of intrinsic acute renal failure in hospitalized patients? | acute tubular necrosis |
| 1. Patient with fever, rash and oliguria after starting a new drug?
2. What is the best initial test? | 1. Allergic interstitial nephritis
2. ↑ WBC on U/A (best is Hansel's stain for eosinophils in urine) |
| 1. Most important initial test to perform in a person who presents with painful muscles and dark urine.
2. Treatment | 1. EKG for possible cardiac complications of hyperkalemia
2. Ca2+, hydration, bicarbonate to alkalinize urine |
| 1. What is the metabolic complication of ethylene glycol overdose?
2. Treatment | 1. formation of toxic metabolic oxalic acid
2. fomepizole followed by dialysis to remove the ethylene glycole |
| 1. Most common cause of acute hyperoxaluria with metabolic acidosis?
2. Most common cause of chronic hyperoxaluria?
2. | 1. ingestion of antifreeze
2. Crohn's disease from fat and calcium malabsorption |
| Mechanism of action of allopurinol | prevents conversion of xanthine to hypoxanthine to uric acid |
| Most common cause of hypercalcemia | hyperparathyroidism |
| What is the difference in presentation between acute interstitial nephritis (AIN) and direct toxins to the kidney? | 1. AIN occurs with the first dose and presents with fever, rash, and eosinophils
2. direct toxins take several days/weeks |
| What is the least nephrotoxic aminoglycoside | tobramycin |
| What is renal insufficiency? | renal failure that is not severe enough to require dialysis; aka azotemia |
| Patient with recent vascular catheter develops signs of renal failure. | atheroembolic disease |
| Which HIV drug is most associated with neprholithiasis? | indinavir (protease inhibitor) |
| Acute flank pain, hematuria, pyuria and fever:
1. patient with + urine cultures
2. patient with history of diabetes, sickle cell or NSAID use
3. What is the most accurate diagnostic test? | 1. acute pyelonephritis
2. papillary necrosis
3. Ct scan |
| Most likely prevention of contrast-induced renal failure. | hydration |
| 1. Patient with edema, hematuria and hypertension
2. What test confirms the diagnosis? | 1. glomerulonephritis
2. renal biopsy |
| 1. Patient with sinusitus and renal disease
2. best initial test
3. most accurate test
4. Treatment | 1. Wegener's granulomatosis
2. C-ANCA
3. biopsy of kidney or nasal septum/lung
4. cyclophosphamide and steroids |
| 1. Patient with chronic asthma, elevated WBC skin lesions.
2. Treatment | 1. Churg-Strauss
2. glucocorticoids and cyclophosphamide |
| What areas of the body are effected by polyarteritis nodosa? | virtually every organ except the lung |
| 1. Palpable purpura with arthralgies
2. What is the pathophysiologic cause
3. Treatment | 1. Henoch-Schonlein purpura
2. systemic deposition of IgA
3. supportive because disease is self-limiting |
| Characteristics of Glomerulonephritis | 1. Edema (low oncotic pressure; Salt and water retention)
2. Hematuria with dysmorphic RB cell (red cell squeeze through the glomeruli)
3. Proteinuria < 2g/24hr
4. Fractional excretion of Na <1% (you are retaining it, you can't be excreting it)" |
| Churg-strauss Syndrome: best lab test? | eosinophilia and positive C-ANCA |
| Churg-Strauss Syndrome: most accurate test | Biopsy |
| Goodpasture Syndrome: best initial test | Antibasement membrane antibodies to type IV collagen |
| Goodpasture Syndrome: most accurate test | lung or kidney biopsy; IF shows linear deposit |
| Goodpasture Syndrome: treatments | plasmapheresis and steroid, +/- cyclophosphamide |
| Polyarteritis Nodosa: best initial test | P-ANCA |
| Polyarteritis Nodosa: most accurate test | biopsy (need angiogram done before bx) |
| Polyarteritis Nodosa: Treatments | cyclophosphamine and steroid |
| Henoch-Schonlein Purpura: Treatments | Steroids if disease is severe or porgressive |
| IgA nephropathy (Berger Disease): best initial test | increase IgA |
| IgA nephropathy (Berger Disease): most accurate test | renal biopsy |
| IgA nephropathy (Berger Disease): Treatments | no effective treatment; steroid won't reverse IgA problem; use ACEI or ARBS for proteinuria |
| Postinfectious Glomerulonephritis: characteristics | Smoky, cola or tea colored urine; due to strep pyogenes, Hep B and C, CMV, chronic staph infections) |
| Postinfectious Glomerulonephritis: best initial test | ASO (antistreptolysin) test or AHT(antihyaluronic acid) test |
| Postinfectious Glomerulonephritis: most accurate test | renal biopsy; EM shows humps of IgG and C3 |
| Postinfectious Glomerulonephritis: Treatments | 1. supportive
2. manage fluid overload and HTN with diuretics |
| Thrombotic thrombocytopenic Purpura: characteristics | Pentad presentation: 1. hemolytic anemia; 2. uremia; 3. thrombocytopenia; 4. fever; 5. neurologic problems |
| Hemolytic uremic syndrome: characteristics | Triad presentation: 1. hemolytic anemia; 2. uremia; 3. thrombocytopenia |
| In Hemolytic uremic syndrome
1. What antibiotics do you give?
2. How do you treat thrombocytopenia? | 1. none; if antibiotics are given, organism may release more toxins as it dies
2. do not transfuse platelets bc they precipitate and worsen the CNS and renal abnormalities |
| 1. crescent formation of glomerulus on biopsy
2. treatment | 1. rapidly progressive glomerulonephritis
2. steroids and cyclophosphamide |
| What are the two common types of amyloidosis? | 1. AL from light chains
2. AA from chronic infection or inflammation |
| What defines nephrotic syndrome? | renal disease sufficient to produce a level of proteinuria greater than 3.5 gram per 24 hours, hyperlipidemia, edema and low serum albumin |
| What is the cause of hyperlipidemia in nephrotic syndrome? | loss of lipoproteins on the surface of chylomicrons and LDL so these lipids are not cleared from the bloodstream |
| Most common form of idiopathic nephrotic syndrome in adults | membranous |
| Cause of casts on urinalysis:
1. hyaline
2. red cell
3. white cell | 1. dehydration
2. glomerulonephritis
3. pyelonephritis |
| Cause of the following casts on urinalysis:
1. broad, waxy
2. granular | 1. chronic renal failure
2. acute tubular necrosis |
| What are the indications for dialysis? | A E I O U
1. Acid/base disorders
2. Electrolytes (↑K)
3. Intoxication
4. Overload of volume
5. Uremia (pericarditis, encephalopathy) |
| Cause of hypocalcemia in renal failure (2)? | 1. low vitamin D
2. high phosphate which precipitates calcium |
| What is used to treat hyperphosphatemia from end-stage renal disease? | phosphate binders:
1. calcium carbonate
2. calcium acetate |
| What is used to treat hyperphosphatemia from end-stage renal disease when calcium mis abnormally high (from vitamin D replacement? | 1. sevelamer
2. lanthanum |
| What happens to the levels of the following electrolytes in ESRD:
1. calcium
2. phosphate
3. magnesium | 1. decreases
2. increases
3. increases |
| 1. What is the suggested blood pressure management for those with ESRD?
2. Why? | 1. <130/80
2. rapidly progressive coronary artery disease is the most common cuase of death |
| 1. How does ESRD lead to bleeding?
2. What is the treatment? | 1. uremia-induced platelet dysfunction
2. desmopressin causes release of subendothelial vWF stores and factor 8 |
| Why can hyponatremia lead to hypertension? | "1. as ECT osmolality decreases, water shifts into brain cells increasing the ICP
2. blood pressure increases to maintain cerebral perfusion pressure" |
| How does hyponatremia effect intracranial pressure? | water shifts into the cells leading to increased ICF volume and thus increased ICP |
| At what level does hyponatremia become symptomatic? | < 125 |
| "What is the treatment for:
1. mild hyponatremia
2. moderate hyponatremia
3. severe hyponetremia | 1. fluid restriction
2. normal saline (0.9%) + loop diuretic
3. 3% hypertonic saline or V2 receptor-antagonist" |
| What neurologic disorder is caused by correcting hyponatremia too rapidly? | central pontine myelinolysis |
| Why may hyperglycemia manifest with pseudohyponatremia? | ↑ glucose osmotically draws water into the vascular space and dilutes sodium |
| Most important diagnostic test when a patient has suspected hypokalemia | EKG |
| What acid base status is seen following dehydration? | volume contraction → ↑ aldosterone → metabolic alkalosis |
| How does replacement of B12 in deficient patients lead to hypokalemia? | potassium is found mostly intracellularly and with rapid cell production from B12, extracellular K+ moves into cells |
| How is magnesium related to potassium metabolism? | magnesium decreases urinary loss of potassium therefor hypomagnesemia leads to hypokalemia |
| Rx for hypovolemia from vomiting? | 1. GI loss of H+ and volume contraction → ↑ aldosterone → H+ loss and HCO3 retention
2. 2. treat contraction alkalosis with IV normal saline with the addition of potassium to replace K+ loss |
| Rx for severe hypercalcemia? | normal saline followed by furosemide |
| How do the following effect calcium levels:
1. acidosis
2. alkalosis | 1. results in hypercalcemia because albumin binds H+ and releases Ca2+
2. results in hypocalcemia |
| Patient with multiple blood transfusions has a seizure and perioral numbness. | hypocalcemia from binding of free calcium to citrate |
| How can alcoholism lead to hypocalcemia | low magnesium from malnutrition prevents the release of parathyroid hormone from the thyroid gland |
| How does hyperglycemia manifest with hyponatremia? | high glucose level causes a transcellular shift of water out of the cell into the vascular space, diluting the sodium |
| Rx for:
1. mild hypovolemic hypernatremia
2. severe hypovolemic hypernatremia | 1. D5 1/2NS
2. D5W |
| Treatment for nephrogenic diabetes insipidus | HCTZ, amiloride, NSAIDs |
| What effect does insulin have on potassium levels? | insulin causes uptake of potassium by cells |
| Patient with muscle weakness and peaked T waves on EKG. What is the treatment? | 1. calcium chloride protects heart
2. insulin + glucose shift K+ into cells
3. Kayexalate removes K from body" |
| "Which fluid should be given:
1. hypovolemia with alkalosis
2. hypovolemia with acidosis | 1. normal saline
2. lactated ringer |
| 1. What is the tonicity of sweat?
2. What are the resulting sodium levels in the body? | sweat is mostly free water (hypotonic) and results in hypernatremia |
| How do you diagnose SIADH? | elevated urine osmolality (>100) in a patient with hyponatremia |
| Treatment for SIADH
1. severe disease
2. chronic disease in which underlying cause can't be corrected | 1. 3% hypertonic saline
2. V2 receptor antagonists (conivaptan and tolvaptan) |
| How fast can hypo or hypernatremia be corrected? | ~ 0.5 mEq per hour |
| How does aldosterone effect K+ concentration? | causes hypokalemia mainly from K+ secretion from colon and small part from kidneys |
| What are the EKG findings of patients with suspected hypokalemia? | T-wave flattening and U-waves |
| What action does Kayexalate have? | resin that absorbs 1 mEq K per g and releases 1 mEg Na |
| 1. Asymptomatic hyperkalemia with nonanion gap metabolic acidosis
2. How do you confirm the diagnosis?
3. Treatment | 1. aldosterone deficiency
2. Presence of high urine sodium with oral salt restriction.
3. Fludrocortisone |
| What electrolyte changes are seen with volume contraction? | 1. K secretion
2. Na+ absorption
3. HCO3 absorption
4. H+ secretion |
| What is the anion gap a measure of? | 1. gauge of the unmeasured anions in the bloodstream
2. positively charged cations - negatively charged anions |
| In normal anion gap metabolic acidosis, how can one determine if the cause is due to renal or intestinal HCO3 loss? | 1. determine urine anion gap (Na + K) - Cl
2. positive gap indicates renal tubular acidosis |
| 1. What are the main cations of the blood?
2. What are the main anions? | 1. Na+, K+, Ca2+
2. HCO3-, Cl-, albumin, lactate, ketoacids |
| What acid/base disturbance do salicylates create? | respiratory alkalosis + metabolic acidosis |
| 1. What is the composition of most renal stones?
2. What electrolyte irregularities increase stone formation? | 1. calcium oxalate
2. increased calcium, decreased oxalate |
| What causes struvite stones? | urinary infections with urease positive organisms |
| Radiolucent stones | uric acid |
| Extra-renal manifestations of adult polycystic kidney disease | 1. hepatic cysts
2. hypertension
3. berry aneurysms
4. mitral valve prolapse |
| What degree of proteinuria distinguishes nephritis from nephrotic syndrome? | >3g/day = nephrotic |
| What is the FeNa in glomerulonephritis? | FeNa < 1 because there is salt and water retention |
| What is the difference between Henoch-Schonlein purpura and IgA nephropathy? | both occur from IgA deposition but IgA nephropathy only effects the kidneys |
| Patient with recent viral illness
1. Develops hematuria 1-2 days later
2. Develops hematuria 1-2 weeks later | 1. IgA nephropathy
2. poststreptococcal glomerulonephritis |
| 1. Why must one biopsy in lupus nephritis?
2. What is the treatment? | 1. to determine if there is sclerosis or proliferative disease
2. sclerosis does not need therapy; proliferative disease is treated with steroids and mycophenolate |
| 1. How is nephrotic syndrome diagnosed?
2. How is the cause of nephrotic syndrome determined? | 1. protein:creatinine ratio of >3.5
2. renal biopsy |
| What is the diagnosis of SIADH based on? | elevated urine osmolality and urine sodium in a patient with hyponatremia |
| 1. Patient with flattened T waves and U waves present
2. What causes the U wave | 1. hypokalemia
2. purkinje fiber repolarization |
| What is the maximum oral dose of potassium? | no max dose because gut cannot absorb it fast enough to overload kills |
| What is the problem in renal tubular acidosis:
1. Type I
2. Type II
3. Type IV | 1. impaired distal secretion of H+
2. impaired proximal absorption of bicarbonate
3. aldosterone deficiency |
| 1. What 2 things cause normal anion gap metabolic acidosis?
2. What laboratory test helps distinguish between the two? | 1. diarrhea and renal tubular acidosis
2. urine anion gap |
| 1. How do you quantify oliguria?
2. How do you quantify anuria? | 1. <400 mL per 24 hours
2. <100 mL per 24 hours |
| 1. When is Winter's formula used?
2. What is Winter's formula? | 1. to determine if the is appropriate respiratory compensation for metabolic acidosis
2. (1.5 x HCO3-) + 8 ± 2 |
