Renal physiology 2 Flashcards
Low anion gap is seen in
Hypoalbuminemia
Multiple myeloma
Distal renal tubular acidosis (type 1) Defect in which cell: pH: Causes: Association:
►Inability of α-intercalated cells to secrete H+→ no new HCO3– is generated metabolic acidosis
► > 5.5
►Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE)
►risk for calcium phosphate kidney stones
RTA type 2
Causes:
Association
►Fanconi syndrome,
multiple myeloma,
carbonic anhydrase inhibitors
►risk for hypophosphatemic rickets (in Fanconi syndrome
Hyperkalemic tubular acidosis (type 4)
Defect
Hypoaldosteronism or aldosterone resistance; hyperkalemia ↓NH3 synthesis in PCT →↓NH4+ excretion
Saline responsive metabolic alkalosis
Hypovolemia: Vomiting, Diuretic use
Saline unresponsive metabolic alkalosis
Bartter & Gitelman syndrome, Excess mineralocorticoid
Effects of diuretics on urinary Cl-
Initial: ↑urinary Cl-
Later: ↓ urinary Cl-
Methanol is metabolized to:
distinguishing symptom:
Formic acid Visual symptoms (retinal damage)
Ethylene glycol is metabolized to:
distinguishing feature:
►glycolate and oxalate
►flank pain & oliguria (these both are kidney toxins)
Lactic acidosis in conditions:
Shock Ischemic bowel Metformin therapy Seizures Exercise
Iron toxicity phases:
Initial GI phase
After 24h: CVS toxicity, coagulopathy, acute lung injury
Weeks later: bowel obstruction due to scarring
Aspirin acid base disorders causes
Early: stimulate medulla → hyperventilation → Respiratory alkalosis
Late: uncouples oxidative phosphorylation and ↓lipolysis → accumulation of pyruvate, lactic acid, ketoacids → metabolic acidosis
Contraction alkalosis mechanism:
►Mechanism of K+ excretion
■ ATII → ↑H+ secretion in PCT, ↑HCO3 resorption in PCT
■ Aldosterone → ↑H+ secretion collecting duct
►Alkalosis → K+ shift into principal cells → ↑Urinary loss of K+
_____ stimulates kidney ammoniagenesis by metabolizing ______
Acidosis
Glutamine
