Potassium depletion nephropathy

Laboratory evaluation of cats with chronic renal failure and presumed potassium depletion shows moderate to severe hypokalemia (usually < 3.1 mEq/L), increased creatine kinase concentration, azotemia, hyperchloremic metabolic acidosis, variable hyperphosphatemia, and isosthenuria. Histopathologic findings observed in the kidneys of cats with chronic renal failure and presumed potassium depletion, include interstitial fibrosis, lymphoplasmacytic interstitial inflammation, tubular dilation, tubular atrophy, and variable glomerular sclerosis. Acute treatment requires diligent potassium supplementation by both oral and intravenous routes. 

Potassium should not be infused intravenously at a rate greater than 0.5 mEq/kg body weight per hour. Infusion of potassium-containing crystalloid fluids initially may be associated with a decrease in serum potassium concentration as a result of dilution, increased tubular fluid flow in the distal renal tubules, and cellular uptake of potassium. This effect may be minimized by selecting a fluid that does not contain glucose, administering fluids at an appropriate rate, and beginning oral potassium gluconate (4 to 8 mEq q24h) as soon as possible. Clinical improvement usually is observed within one to three days. Chronic treatment involves oral administration of potassium gluconate (2 to 4 mEq q24h). Treatment results in resolution of muscle weakness, hypokalemia, and anaemia. Renal function stabilizes or improves in most instances.