Missed Renal Qs

1. Post-infectious glomerulonephritis: Post-infectious glomerulonephritis is typically seen within two weeks of a group A beta-hemolytic streptococcal infection and presents with oliguria, edema, hypertension and smokey-brown urine. Look for low serum C3, an increased ASO titer and lumpy-bumpy immuno-fluorescence. Treatment involves supportive measures only as most patients will have complete recovery.

IgA nephropathy: IgA nephropathy is highly associated with upper respiratory or gastrointestinal infections and is classically seen in young males. Episodic frank hematuria occurs in nearly 40% of all cases and usually starts within a day of an upper respiratory tract infection (as opposed to post-streptococcal glomerulonephritis, which typically occurs around two weeks after infection with group A beta-hemolytic streptococcus). The frank hematuria often resolves after a few days, however the microscopic hematuria persists. IgA nephropathy occurs due to deposition of the IgA antibody in the glomerulus. Henoch-Schönlein purpura is highly associated with IgA nephropathy and is thought to be a systemic form of the disease. Henoch-Schönlein purpura presents with “palpable purpura” and is commonly seen in young adults ages 16-35.

Wegener’s granulomatosis: Wegener’s granulomatosis is a type of vasculitis that presents in various ways, though persistent URI symptoms (e.g. rhinitis) is the initial presenting symptom in most cases. Look for upper-airway, eye and ear disease along with rapidly progressive glomerulonephritis that leads to chronic renal failure. Wegener’s can also manifest with skin, arthritic, and neurological changes as well. The presence of c-ANCA can aid in the diagnosis, but is still a non-specific finding. Treatment usually begins with corticosteroids and oral cyclophosphamide.

Goodpasture’s syndrome: Goodpasture’s syndrome is a rare condition characterized by acute glomerulonephritis and pulmonary alveolar hemorrhage. This condition is also referred to as a pulmonary-renal syndrome. The most common presentation is hemoptysis or cough in the presence of gross hematuria. Look for the presence of anti-GBM antibodies. Treatment includes plasma exchange and immunosupression with corticosteroids and cyclophosphamide.

Alport’s syndrome: Alport’s syndrome is a genetic disorder (X-linked in 80% of cases) characterized by the progressive loss of kidney function and sensorineural hearing impairment that commonly occurs during late childhood or early adolescence. There is usually a strong family history of hematuria, which is the most common presentation in patients suffering from the disorder.

2. Intrinsic renal failure in the setting of infection and shock is most likely caused by sepsis due to hematogenous spread of infection. Antibiotics can cause acute renal failure but is less likely in the setting of hypotension and fever. Toxic shock syndrome can also cause acute renal failure but is less likely a complication of pneumonia in an elderly nursing home patient. Toxic shock syndrome complicates gram positive infections most commonly of the skin and vagina.
3. In the early part of an asthma exacerbation, the patient has not become fatigued and is able to compensate for increase in work required for adequate oxygen delivery → Respiratory Alkalosis.
1. Respiratory Acidosis is not seen until the muscles of respiration begin to fatigue, as would be the case in a severe and prolonged asthma exacerbation.
4. Nephrotic syndrome is associated with a hypercoagulable state.
5. Cryoglobulinemia presents with GN and decreased C3/C4 levels.
1. The pathology involves immune complexes, containing antibodies and complement protein, being deposited in the glomeruli and subsequently initiating an inflammatory response. It is commonly associated with IV drug abusers and patients with chronic hepatitis B and/or C.
2. In GN caused by IgA nephropathy the complement levels are normal.
3. Wegener syndrome can also present with GN but the complement levels are normal.
6. Renal tubular acidosis type II is associated with defects in proximal tubular reabsorption.
1. Characterized by
1. ↓ serum bicarbonate
2. ↑ high urine bicarbonate due to defects in proximal tubular reabsorption.
3. Glucose is also reabsorbed in the proximal tubule and thus may be found in the urine (Fanconi syndrome)
2. These patients are also at increased risk for bone diseases like multiple myeloma and osteomalacia.
3. All types of renal tubular acidosis are characterized by normal anion gap metabolic acidosis.
4. RTA I is a/w urine pH >5.5
1. At risk for renal stones
5. RTA IV is a/w hyperkalemia - d/t aldosterone insufficiency or resistance.
7. Bumetanide is the best orally available of the diuretics listed. It is the loop diuretic with the best absorption.
1. Ethacrynic acid is the only loop diuretic safe for use in people with sulfa allergies.
2. Mannitol is an osmotic diuretic, not a loop diuretic (hint: question is about a patient in heart failure). Additionally, mannitol is not orally bioavailable and must be administered IV.
8. First line treatment for IgA nephropathy is the combination of ACE inhibitor and ARB. This combination is effective for both proteinuria and hypertension. If there is progressively active disease despite ACE inhibitor/ARB therapy, prednisone can be added to the regimen.
9. Magnesium replacement is crucial in the treatment of patients suffering from alcohol withdrawal. Many patients with chronic alcoholism have clinically significant magnesium deficiency secondary to malnutrition and chronic diuresis from alcohol ingestion. Symptoms of hypomagnesemia are similar to those of alcohol withdrawal and include tachycardia, seizures, tremor, and hyperreflexia. Replacement with magnesium sulfate decreases total sedation required and decreases incidence of seizures.
10. Chronic hypertension is a strong risk factor for left-sided congestive heart failure.
11. Renal tubular acidosis type 1 is associated with hypokalemia and high urine pH with a predisposition for kidney stones.
1. In this condition hydrogen ions are not properly excreted in the urine leading to acidosis and high urine pH (generally greater than 6). These patients tend to have elevated urine calcium and a predisposition to renal stones. Excess vomiting leads to metabolic alkalosis (A). Diarrhea leads to a normal anion gap acidosis with a negative urine anion gap (kidneys compensate for the loss of bicarbonate with excess NH4+ and CL- excretion)
2. Fanconi syndrome is characterized by a defect in proximal tubule reabsorption leading to glucose, amino acids and bicarbonate excretion in the urine. This is associated with renal tubular acidosis type 2, where the urine pH is generally not as high as found in type 1 and could even be acidic
3. Adrenal insufficiency is associated with renal tubular acidosis type 4 which is characterized by hyperkalemia
12. SIADH causes a euvolemic hyponatremia that most commonly presents without edema or changes in blood pressure.
1. SIADH causes the retention of free water without a change in plasma volume (euvolemic hyponatremia), thus blood pressure generally remains normal. Excess ADH → concentrated urine.
1. Hyponatremic euvolemic.
2. Hyperkalemia coupled with hyponatremia suggests adrenal failure
13. When the kidney does not receive the amount of perfusion that it deems to be adequate in situations like hypovolemia and decreased cardiac output then the renin- angiotensin-aldosterone system activates causing retention of sodium and a tubular secretion of potassium.
1. during CHF there is a decrease in effective circulating volume. Therefore the kidney will increase the tubular absorption of sodium and decrease the amount of sodium in the urine <20meq/24hours.
2. There is an increase in chloride excretion in patients taking steroids but not people whom are in CHF
14. Urinary casts with dysmorphic red blood cells is highly suggestive of glomerular disease.
1. Acute tubular necrosis is associated with muddy brown casts of epithelial cell origin
15. A low protein diet is recommended for all types of kidney stones.
1. Neither high/low calcium diet is not recommended for calcium stones and in fact may exacerbate the condition.
2. High urine pH exacerbates calcium stones.
3. Antibiotics may be useful for struvite stones which occur in patients with recurrent urinary tract infections.
1. Infection with Proteus spp. and Klebsiella spp. (urease producing organisms) can cause struvite stones, which can proceed to staghorn stones involving large portions of the renal collecting system.
4. Shock wave lithotripsy is not necessary for stones less than 5-mm in diameter.
5. Cystine stones are much less likely, develop in patients with an autosomal recessive disorder.
1. Cystine renal stones are caused by a genetic defect in amino acid transport and are associated with acidic urine.
16. Eosinophiluria, eosinophilia, low grade fevers, mild proteinuria, and arthralgias, in the setting of exposure to medication, should raise your suspicion for Acute Interstitial Nephritis (AIN). The most important treatment is to stop the offending agent.
1. Drug induced acute interstitial nephritis can be caused by several medications including
1. penicillins, cephalosporins, rifampin, sulfa drugs, quinolones, NSAIDs, diuretics, allopurinol, and phenytoin.
2. Treatment of AIN requires cessation of the offending drug and observation to see if symptoms resolve.
3. If symptoms do not improve, the next step in management would be to consider a trial of steroids.
4. The definitive test for diagnosis of AIN is kidney biopsy, but this is only utilized when clinical diagnosis is difficult, due to its invasive nature.
17. A renal ultrasound must be performed in patients with BPH and an elevated creatinine to evaluate for hydronephrosis and bladder outlet obstruction.
18. The most common medical causes of nephropathy are diabetes and hypertension.
1. Pre-renal azotemia can cause elevations in BUN and Cr but signs/symptoms of dehydration should also be present; also, the case states that this patient has a history of HTN and this should lead you in the direction of hypertensive nephropathy.
19. Renal artery stenosis presents with hypertension and an abdominal bruit. These patients are at risk for hypokalemia.
1. Checking electrolytes is important because hypokalemia can result from the high renin levels.
2. A renal ultrasound is NOT the best imaging choice for renal artery stenosis. Angiography is best to confirm the diagnosis but is usually only done when surgery or angioplasty is being considered
3. This patient is presenting with signs and symptoms most consistent with renal artery stenosis. The clues to this diagnosis include hypertension, muscle weakness and an abdominal bruit. In young patients, this is commonly caused by fibromuscular dysplasia.