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
Best initial test and most accurate test for proximal renal tubular acidosis
- Best initial: Urianalysis➡Variable pH; Basic at first (>5.5), until most HCO3 is lost, pH <5.5
- Most accurate: Give HCO3 and test urine pH➡⬆⬆urine pH
Treatment for proximal renal tubular acidosis
Thiazide➡volumen depletion➡⬆HCO3 absorption
Complication of proximal renal tubular acidosis and why does it happen?
Acid can’t be excreted into de the tubule➡⬆Urine pH (alkaline urine)➡⬆formation of calcium oxalate stones in kidneys
Treatment of renal tubular acidosis type IV
Fludrocortisone➡”Aldosterone like” effect
Which drug may help to avoid the recurrence of calcium kidney stones?
Hydrochlorothiazide➡⬆distal tubular reabsorption of Ca➡removes Ca from urine
Treatment for distal renal tubular acidosis
Replace HCO3-➡will be absorbed in the proximal tubule
Mechanism of renal dysfunction in an end-stage liver disease
Hepatorenal syndrome➡splanchnic arterial dilation ➡⬇vascular resistance➡➕RAAS➡local renal vasoconstriction (renal arterioles)➡⬇perfusion and glomerular filtration
Best next step when unilateral varicoceles fail to empty when a patient is recumbent
Suspicion of underlying mass (eg, Renal cell carcinoma)➡obstructs venous flow▶CT scan of the abdomen
Mechanism of calcineurin inhibitor toxicity (tacrolimus, cyclosporine). Most common toxicities.
Vasoconstrictive properties
- Acute: Hypertension and AKI [prerenal] (constriction of afferent and efferent arteriole, reversible)
- Chronic: slow decline in renal function (prolonged vasoconstrictive renal ischemia, tubular toxicity, irreversible)
*Elicit by impairment in hepatic clearance (Ex, add drugs metabolized by cytochrome P450)
Which test might detect eosinophils in the urine? What may suggest?
Wright and Hensel stains➡Allergic interstitial nephritis
*Most accurate test for AIN
What is Isosthenuria and why does it happen?
- Urine Osmolality similar to blood Osmolality (about 300 mOsm/L)
- Acute tubular necrosis➡tubule cells cannot reabsorb water
*Renal tubular concentrating defect
Most probable cause of acute kidney injury in a patient with hematologic malignancy who is beginning chemotherapy
Tumor lysis syndrome➡hyperuricemia
How do you prevent renal failure from tumor lysis syndrome?
Give prior chemotherapy: Allopurinol, hydration and rasburicase
What type of kidney damage may cause rhabdomyolysis and why?
⬆Myoglobin➡severe oxidant stress on the tubular cells▶Acute tubular necrosis
Best initial and most specific test for rhabdomyolysis during ATN
- Best initial: ⬆⬆blood on urine dipstick, no RBC on microscopic examination
- Most: Urine myoglobin
Which electrolyte disturbances might be identified in rhabdomyolysis?
Hyperkalemia
Hyperuricemia
Hyperphosphatemia
Hypocalcemia (⬆Ca binding to damaged muscle)
Treatment for rhabdomyolysis
- Saline hydration
- Mannitol➡osmotic diuretic
Most common medications causing acute (allergic) interstitial nephritis
- Penicillins and cephalosporins
- Sulfa drugs (include furosemide and thiazide)
*Drugs overall are the cause in 70% of cases
Most likely clinical presentation of acute (allergic) interstitial nephritis
- Acute renal failure
- Fever (80%)
- Rash (50%)
- Arthralgias
- Eosinophilia and Eosinophiluria (80%)
- ⬆BUN:Creatinine (but <20)
- 10% of patients have simultaneously all the findings
- Urine eosinophils not found in AIN from NSAIDs
Treatment for acute interstitial nephritis
- Stop drug or control infection➡usually resolves spontaneously
- Severe disease➡Dialysis
- ⬆⬆creatinine even stopping drug➡Glucocorticoids
Most accurate test for papillary necrosis
CT Scan➡abnormal internal structures of the kidney from the loss of the papillae
What is postictal lactic acidosis and how do you manage it?
- Anion gap metabolic acidosis typically following tonic-clonic seizure➡skeletal muscle hypoxia, ⬇hepatic lactic acid uptake▶⬆⬆lactic acid
- Transient and self-limited in 90 minutes➡observe and repeat chemistry in 2 hours
How do you suspect an acute renal allograft rejection? How do you confirm it?
- Typically within the first 6 months after a transplant
- Asymptomatic usually
- Acutely ⬆creatinine, proteinuria
- Confirmation by Bx➡Lymphocytic infiltration of the intima, inflammatory tubular disruption, intimal arteritis.
- Mostly Reversible (⬆dose glucocorticoids)
How do the calcineurin inhibitors cause acute toxicity to kidneys? What do you expect to find?
Vasoconstriction of afferent and efferent renal arterioles➡prerenal acute kidney injury and hypertension
When do you suspect a BK virus reactivation in a patient with a renal transplant? What is the finding in the most accurate test?
- Excessive immunosuppression in renal allograft recipients➡tubulointerstitial nephritis
- Asymptomatic ⬆creatinine
- Bx➡intranuclear inclusions, mixed lymphocytic and neutrophilic infiltrate
Common findings on urinalysis in a patient with glomerulonephritis
- Hematuria
- Dysmorphic red cells
- Red cell casts
- Proteinuria
Treatment of nephrogenic diabetes insipidus
- Correct potassium and calcium
- Stop lithium or demeclocycline
- Hydrochlorothiazide or NSAIDs (still having NDI despite previous interventions)
Best initial and most accurate test for distal renal tubular acidosis (Type I)
- Best initial: Urinalysis➡⬆pH>5.5
- Most accurate: infuse acid (ammonium chloride)➡urine pH remains basic >5.5. Normal response is ⬇pH
In addition to drugs, which other cause of acute interstitial nephritis there might be?
- Autoimmune diseases (20%): SLE, Sjögren, Sarcoidosis
- Infections or Idiopathic (10%)
Best next step in management when a male patient has a penile fracture and suspects urethral injury
Retrograde urethrography (urethroscopy)➡rule out urethral injury (20% of PF) before surgery
*Possible urethral injury: urinary retention/blood at the meatus/hematuria/dysuria
What additional studies do you do on adult patients with membranous nephropathy?
- Hepatitis B serology, HCV, syphilis, studies for autoimmune disease, malignancy because evaluation for secondary causes should be done in adults
- MN is often idiopathic or primary
