Renal/Genitourinary Flashcards
Best diagnostic study for evaluating and confirming the diagnosis of bladder cancer
Cystoscopy
Treatment of urinary uric acid stone
- Hydration
- NSAIDs (pain killers)
- Potassium citrate or potassium bicarbonate→alkalinization of urine►uric acid stone dissolve in an alkaline medium
- Add allopurinol if stones don’t resolve with initial treatment
- Radiolucent stones
Why you should avoid sodium bicarbonate for a uric acid stone treatment?
Extra salt load→volume expansion►hypercalciuria→formation of calcium stones
*Uric acid is a nidus for calcium oxalate stone formation
Which electrolyte disturbance is caused by Bartter syndrome? Look like which pharmacologic effect?
- Reabsorptive defect in thick ascending loop of Henle→Affect K/Na/Cl cotransporter►hypokalemia, metabolic alkalosis, hypercalciuria
- Chronic loop diuretic use
Treatment for Bartter syndrome
- Spironolactone→antagonizes effect of ↑aldosterone (↑ by the loss of electrolytes and intravascular volume in Bartter)
- NSAID→↓excessive prostaglandins (in Bartter ↑PGE)
Potential cause of low urine specific gravity and normal serum sodium
Hyposthenuria➡Sicke cell disease or sickle cell trait▶hypoxic, hyperosmolar condition of the renal medulla➡RBC sickle in the vasa recta➡❌water reabsorption and countercurrent exchange
When do you use acute therapy for hyperkalemia?
- ECG changes
- K>7 mEq/L (with or without ECG changes)
- Rapidly rising K due to tissue breakdown
- Dialysis→renal failure or severe life-threatening hyperkalemia unresponsive to initial therapy
- Calcium gluconate and insulin with glucose
Which metabolic disturbance can be found on diabetic hyporeninism? why?
- Hyperkalemic metabolic acidosis
- Damage of the juxtaglomerular apparatus→hyporeninemic hypoaldosteronism►”aldosterone deficiency”→Renal tubular acidosis type IV (hyperkalemic RTA)
Pathophysiology of renal tubular acidosis type IV (hyperkalemic RTA) and its metabolic consequence
- Aldosterone insufficiency→Diabetic hyporeninism, ACEI, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency
- Aldosterone resistance→K sparing diuretics, obstructive nephropathy, TMP/SMX
- *Impaired function of the cortical collecting tubule►retention of H and K→hyperkalemic Non-anion gap metabolic acidosis
- Preserved kidney function→at least 20-50 mL/min
Which electrolyte disturbance can occur due to immobilization and its mechanism?
- Hypercalcemia
- ↑Osteoclastic bone resorption
*Onset around 4 weeks, patients with chronic renal insufficiency develop it in about 3 days
Mechanisms by which Beta-adrenergic agonists cause hypokalemia
- Stimulate Na-K ATPase pump and the Na-K-2Cl cotransporter→potassium shift into the intracellular space
- Release of Insulin→promotes intracellular K+ shift
Most appropriate initial step in the management of Hyperkalemia with ECG changes
Calcium gluconate
Most common cause of Glomerulonephritis in adults
IgA Nephropathy
Extrarenal complications of autosomal dominant polycystic kidney disease. What is the most common?
- Hepatic cyst
- Intracranial berry aneurysm (5-15%)
- Valvular heart disease (most often mitral valve prolapse and mitral regurgitation)
- Colonic diverticula
- Abdominal wall and inguinal hernia
Which types of acid-base disorder may cause acute kidney injury and why?
- Non-anion gap metabolic acidosis⇦impaired acid excretion, ammonia generation or bicarbonate reabsorption
- Anion gap metabolic acidosis⇦retention of unmeasured uremic toxins
Pathophysiologic mechanism of membranoproliferative glomerulonephritis
- Dense intramembranous deposits that stain for C3
- Deposit disease▶IgG antibodies (C3 nephritic factor) against C3 convertase➡persistent activation of the alternative complement pathway▶kidney damage
What do you have to monitor closely after initiation of Erythropoietin in a CKD patient, and why?
- Blood pressure monitoring
- Up to 30% patients develop new or worsening hypertension 2-8 wks after initiation
*Large doses or rapidly Hb increase, highest risk
In addition to the classical triad of Renal cell carcinoma, what other features you may find?
- Unintentional weight loss
- Intermittent fever
- Paraneoplastic syndromes (ectopic EPO, hypercalcemia)
How do you expect to find the urinary sodium, fractional excretion of sodium, urine sediment, urine WBC and BUN/creatinine ratio in a patient with sepsis?
- Renal hypoperfusion➡activation of RAAS➡⬆Na reabsorption➡⬇Urinary sodium (<20mEq/mL), ⬇Fractional excretion of Na (<1%)
- No intrinsic kidney damage➡urine sediment bland (acellular, no WBC or RBC)
- Urea follows reabsorption of Na and water➡⬆BUN/creatinine ratio >20:1
How are the urinary sodium, urine osmolality and urine sediment in acute tubular necrosis?
- ❌reabsorption of Na by the injured tubules➡⬆Urinary Na (>20mEq/mL)
- ⬇Urine Osmolality (300-350)
- Muddy brown granular urinary casts
- BUN/creatinine ratio 10-15:1
- FENa>2%
*Contrast-induced ATN may have ⬇Urinary Na (<20mEq/mL)
Urine sodium and urine sediment on glomerulonephritis
- RBC casts, mild ⬆WBC, hematuria
- ⬇Urine Na (<20mEq/mL)
*Hypertension
Which conditions may present with very high urinary sodium levels?
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Diuretics
What can damage the renal distal tubule? What is the consequence?
- Drugs: Amphotericin, Topiramate
- Autoimmune diseases: SLE, Sjögren syndrome
- Distal Renal Tubular Acidosis (Type I)➡❌H+ secretion
What can damage the renal proximal tubule? What is the consequence?
- Amyloidosis, myeloma, Fanconi syndrome, acetazolamide, heavy metals, Tenofovir
- Proximal Renal Tubular Acidosis (Type II)➡❌HCO3- reabsorption
