section name header

Table 143-2

Transport Dysfunction in Tubulointerstitial Disease

DefectCause(s)
Reduced GFRaObliteration of microvasculature and obstruction of tubules
Fanconi syndromeDamage to proximal tubular reabsorption of solutes, primarily glucose, amino acids, and phosphate; may also exhibit hypouricemia, proximal tubular acidosis, low-molecular-weight proteinuria
Hyperchloremic acidosisa1. Reduced ammonia production (CKD) or excretion (hyperkalemia)
2. Inability to acidify the collecting duct fluid (distal renal tubular acidosis)
3. Proximal bicarbonate wasting (proximal RTA)
Polyuria, isothenuriaaDamage to medullary tubules (thick ascending limb and/or collecting duct) and vasculature
Hypokalemic alkalosisDamage or hereditary dysfunction of the thick ascending limb or distal convoluted tubule (Bartter's and Gitelman's syndromes)
Magnesium wastingDamage or hereditary dysfunction of the thick ascending limb or distal convoluted tubules
HyperkalemiaaPotassium secretory defects including aldosterone resistance
Salt wastingDistal tubular damage with impaired sodium reabsorption

aCommon.

Abbreviations: CKD, chronic kidney disease; RTA, renal tubular acidosis.