Metabolic causes of chronic tubulointerstitial nephritis

What are the metabolic causes of chronic tubulointerstitial nephritis?

• Oxalate nephropathy

• Dietary: Star fruit, rhubarb, peanuts, and black tea contain high levels of oxalate and are known to cause oxalate nephropathy when consumed in large quantities. Vitamin C is metabolized to oxalate, and thus high doses of vitamin C may also cause oxalate deposition in the kidney.

• Enteric hyperoxaluria: This occurs when there is fat or bile acid malabsorption. The free fatty acids bind to calcium and thereby decrease the availability of calcium to bind to oxalate. Free soluble oxalate is then absorbed in the gut and excreted by the kidney. The most common causes of enteric hyperoxaluria are inflammatory bowel disease, Roux-en-Y gastric bypass surgery, and pancreatic insufficiency.

• Ethylene glycol toxicity results in the formation of calcium oxalate crystals that precipitate in the kidney tubules.

• Genetic: Primary hyperoxaluria types 1, 2, and 3 are each caused by a different enzyme deficiency that leads to the overproduction of oxalate. This leads to nephrocalcinosis, kidney stones, and/or tubulointerstitial disease. When the glomerular filtration rate (GFR) decreases to less than 30 to 45 mL/min per 1.73 m , plasma levels of oxalate exceed saturation and oxalate deposits in other tissues.

• Hypercalcemia/hypercalciuria: Hypercalcemia (resulting from hyperparathyroidism, sarcoidosis, multiple myeloma, etc.) affects the kidney in a variety of ways.

• NDI: This may occur secondary to tubulointerstitial injury and disruption of the interstitial osmotic gradient. Furthermore, activation of the calcium-sensing receptor may also affect the osmotic gradient by decreasing sodium chloride absorption in the loop of Henle.

• Vasoconstriction.

• Distal (type 1) RTA.

• Nephrolithiasis.

• Hypokalemia: Chronic hypokalemia is associated with proximal tubular cell vacuolization, dilated intercellular spaces, and medullary cysts; this clinically correlates with impaired ability to concentrate urine (NDI) and conserve salt, and with the development of hypertension. However, it remains unclear how often chronic tubulointerstitial nephritis occurs secondary to chronic hypokalemia.

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