Tubulointerstitial diseases constitute a diverse group of acute and chronic, hereditary and acquired disorders involving the renal tubules and supporting structures (Table 146-1 Principal Causes of Tubulointerstitial Disease of the Kidney). Functionally, they may result in a wide variety of physiologic phenotypes, including nephrogenic diabetes insipidus (DI) with polyuria, non-anion-gap metabolic acidosis, salt wasting, and hypo- or hyperkalemia. Azotemia is common, owing to associated glomerular fibrosis and/or ischemia. Compared with glomerulopathies, proteinuria and hematuria are less dramatic, and hypertension is less common. The functional consequences of tubular dysfunction are outlined in Table 146-2 Transport Dysfunction in Tubulointerstitial Disease.