Annoying Renal Shit Flashcards
Fanconi Syndrome?
Reabsorptive defect in PCT. Increased excretion of all amino acids, glucose, HCO3-, and PO4. Metabolic acidosis (no more H+ excretion in exchange for bicarb reabsorption). Caused by Wilson’s disease, ischemia, and nephrotoxins
Bartter syndrome?
Reabsorptive defect in TAL. AR. Fucks with Na/K/2Cl transporter. Hypokalemia, metabolic alkalosis (K+ pumped out of cells in exchange for H+ into cells). hypercalciurea
Gitelman syndrome?
Reabsorptive defect of NaCl in DCT. AR. less severe than Bartter. hypokalemia and metabvolic alkalosis with w/o hypercalciuria. tx with K+ sparing diuretics
Liddle syndrome?
inc Na+ reabsorption in DCT and collecting tubules. AD. Hypertension, hypokalemia, metabolic alkalsosis, decreased aldosterone. Tx: amiloride/triamterene
What type of metabolic disorders are the result of renal tubular acidosis
Non-anion gap hyperchloremic metabolic acidosis
Type 1 RTA?
defect in alpha intercalated cells. Cannot secrete H+, so no new bicarb is generated. Hypokalemia (K+ is excreted to maintain urine electroneutrality), inc risk of calcium phosphate kidney stones. Due to amphotericin B, analgesic nephropathy, congenital anomalies/obstruction of the urinary tract
What is the pH of the urine in type I RTA?
pH>5.5 because the rest of the tubules are unable to acidify the urine
Type 2 RTA?
Defect in proximal tubule HCO3- reabsorption. Urine will still be acidic because the alpha intercalated cells downstream are still functioning. Hypokalemia, and increased risk of hypophosphatemic rickets. Caused by fanconi syndrome (wilson’s disease), chemical toxic to proximal (lead, aminoglycosides) carbonic anhydrase inhibitors. Multiple myeloma
Type 4 RTA?
Hyperkalemic! Hypoaldosteronism, aldosterone resistance, or K+-sparing diuretics. Hyperkalemia impairs ammoniagenesis in teh proximal tubule leading to decreased buffering capcity and decreased H+ excretion into urine
