Flashcards in Renal & Electrolytes Deck (51):
Treatment of patients with severe hypovolemic hypernatremia
1st correct the hypovolemia with 0.9% saline.
Then switch to 0.45% saline + 5% dextrose to correct the hypernatremia no faster than 1mEq/L/hour
Earliest renal abnormality in patients with diabetes? Earliest observable abnormality in these patients?
Earliest abnormality = glomerular hyperfiltration
Earliest observable abnormality = GBM thickening
Imaging modalities of choice for patients with suspected kidney stones
Non contrast helical CT and ultrasound (preferred if alternate dx is unlikely or pregnant)
Treatment of choice for uric acid stones
Alkalinization of the urine to a pH of 6 to 6.5 with potassium citrate.
Stones not observable on imaging
Most common type of nephrotic syndrome where you see renal vein thrombosis?
Differentiating benign renal cysts from malignant renal cysts
Simple: smooth, homogenous, do not enhance with contrast, asymptomatic and unilocular.
Malignant: thick, irregular walls, loculated, heterogenous, enhance with contrast, cause pain/hematuria/HTN
Most common causes of anion gap metabolic acidosis
Appropriate rate of correction of serum sodium for patients with hyponatremia
No more than 0.5mEq/dL/hr and not exceeding 12mEq in 24 hours.
How to calculate serum osmolarity
2Na + BUN/2.8 + Glc/18
Calculate serum osmolar gap
Measured Sosm - Calculated Sosm. This is typically done when you suspect ethanol, methanol or ethylene glycol toxicity.
Diagnostic criteria for SIADH
Una > 20
Absence of hypovolemia
Normal renal, adrenal and thyroid function
No obvious stimulus to activate the neuroendocrine hormonal response that increases ADH secretion
Absence of other known causes of hyponatremia
Why is metabolic acidosis due to renal disease rarely seen in patients with an eGFR > 20?
The remaining nephrons compensate greatly for decreased H+ secretion by increasing NH3 production that gets secreted in the urine as NH4 to get rid of the H+.
Dietary recommendations for patients with renal calculi?
Increased fluid to >2L urine/day, decreased Na+ to
Definitive measures used to reduce serum K+
Cation exchange resins like sodium polystyrene sulfonate
How to confirm the diagnosis of cystinuria in a patient with stones?
Hexagonal crystals and urinary cyanide nitroprusside test showing elevated cystine levels.
Post-void residual volume that is significant for bladder outlet obstruction
> 50 mL
Complete vs. partial DI
Complete: urine osmolarity is > 600
Partial: urine osmolarity is 300-600
Common causes of nephrogenic DI
Hypercalcemia, hypokalemia, tubulointerstitial renal disease, Li, demeclocycline, foscarnet, cidofovir and amphotericin
Why do saline-resistant causes of metabolic alkalosis have a high urine Cl- concentration?
Excess mineralocorticoid stimulation results in excess serum Na+ and volume retention. The kidneys respond by secreting more Na+ and Cl-, resulting in increased Cl- concentration.
Treatment of UTIs and pyelonephritis in non-pregnant women?
Acute uncomplicated cystitis: nitrofurantoin x 5 days (avoid if GFR 20%). Fosfomycin x1. Culture urine only if treatment fails.
Complicated cystitis: fluoroquinolones 5-14 days. Amp-gent for more severe cases. Culture urine to confirm correct antibiotic choice.
Pyelo: fluoroquinolones as outpatient therapy. IV fluoroquinolones or aminoglycoside +/- ampicillin for inpatient therapy. Culture urine to confirm correct antibiotic choice.
What constitutes a case of complicated cystitis?
DM, CKD, pregnancy, immunocompromised, urinary tract obstruction, hospital-acquired infection, procedure-associated infection or catheter-associated infection.
Management of hypercalcemia?
Severe (sx or Ca > 14): NS at 200mL/hr with goal urine output of 100-150mL/hr + calcitonin immediately. Give bisphosphonates for long-term treatment.
Moderate (Ca 12-14): no treatment
Tests to get in patients with BPH
Urinalysis and PSA if life expectancy is > 10 years
Most common type of kidney stone
Acid-base abnormality seen with chronic vomiting
Hypochloremic, hypokalemic metabolic alkalosis. This is because for each H+ lost in vomit, one HCO3- is formed. Additionally, hypovolemia leads to RAAS activation, H+/K+ wasting and HCO3- retention.
Common extrapulmonary manifestations of Tb
Liver disease, splenic infiltration, renal disease, Pott's disease and adrenal insufficiency (very common in endemic regions).
NSAID effects on kidneys
Prostaglandin inhibition prevents afferent arteriole dilation and can cause renal failure.
Also, it potentiates the action of ADH and can cause SIADH.
ECG characteristics in hyperkalemia
Peaked T-waves, short QT, long PR and wide QRS that can progress to sine wave morphology.
Kidney stones that will likely pass spontaneously
Most common histology seen in patients with diabetic nephropathy?
Most common causes of nephrotic syndrome in adults with no evidence of systemic disease?
Membranous nephropathy and FSGS
How do you know a patient has FHH vs. primary hyperparathyroidism?
They have very low urine Ca ( 0.02 due to high urinary Ca levels.
Factors that may precipitate hepatorenal syndrome
Those that reduce renal perfusion or GFR
How to diagnose hepatorenal syndrome
Confirm renal hypoperfusion with FeNa
Nephrotic range proteinuria, hematuria and dense intramembranous deposits that stain positive for C3
Membranoproliferative GN. This is due to IgG antibodies against C3 convertase that constitutively activate C3 and the alternative complement pathway.
Muddy brown granular casts
Broad and waxy casts
Muddy brown granular casts - ATN
RBC casts - GN
WBC casts - AIN, pyelo
Fatty casts - nephrotic syndrome
Broad and waxy casts - chronic renal failure
Cardinal features of nephrotic syndrome
Proteinuria (glomerular injury), hypoproteinemia, hyperlipidemia (increased liver synthesis of albumin and lipids), edema (decreased oncotic pressure), hypercoaguability (loss of AT III and increased protein C/S) and hypovolemia
Drugs that commonly cause interstitial nephritis?
Cephalosporins, PCN, sulfonamides, sulfa diuretics, NSAIDs, rifampin, phenytoin and allopurinol.
Antibiotic that can cause hyperkalemia by blocking the eNaC and decreases creatinine secretion?
Characteristics of interstitial cystitis? Treatment?
Bladder pain with filling that is relieved by voiding with no other attributable cause for > 6 weeks. Treat by avoiding triggers + amitriptylene and analgesics during flares.
Why are loop diuretics associated with metabolic alkalosis?
They increase Na delivery to the DCT. This leads to increased Na resorption and K/H secretion -> metabolic alkalosis.
How to prevent at-risk patients from getting contrast-induced nephropathy if they really need imaging done.
Adequate IV hydration with isotonic NaHCO3 or 0.9% NS + acetylcysteine.
Extra-renal manifestations of ADPKD
Abdominal wall/inguinal hernia
Aspects of patients on dialysis that increase their risk of dying from heart disease?
Elevated homocysteine levels
Hyperphosphatemia w/elevated PTH levels
Accelerated atherogenesis from enhanced oxidant stress
Enhanced Ca intake
Patient has gross hematuria, low serum C3 and subepithelial humps consisting of C3 complement on renal biopsy
AA amyloidosis vs. AL amyloidosis
AA = chronic inflammatory conditions, beta-2 microglobulin, apolipoprotein or transthyretin gets abnormally folded and deposited.
AL = MM, Waldenstroms. Lambda light chains get deposited.
Nephritic syndromes with associated low C3 levels
Post-strep GN, lupus, MPGN, mixed cryoglobulinemia
Immune complexes that form in mixed cryoglobulinemia
IgM complexes with anti-HCV IgG, HCV RNA and complement.
Drugs that can cause crystal-induced nephropathy
Acyclovir, sulfonamides, MTX, ethylene glycol and protease inhibitors