renal tubular disease
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Etiology
- hereditary disorders (see hereditary renal tubular defects)
- acquired disorders
- pharmaceuticals nephrotoxic to renal tubules
- exposure to toxins
- renal tubular injury may occur via chronic interstitial nephritis
- aristolochic acid
- germanium
- heavy metals: lead
Pathology
- patterns of renal tubular injury[1]
- tubular proteinuria < 1.5-2 g/day
- proximal tubule dysfunction
- distal tubule dysfunction
- hyperchloremic acidosis*
- hyperkalemia or hypokalemia
- salt wasting
- medullary concentration dysfunction
- nephrogenic diabetes insipidus with decreased urine concentrating ability
- azotemia (renal insufficiency)
- transport dysfunction of renal tubular injury[2]
- reduced GFR*
- obliteration of vasculature
- obstruction of renal tubules
- Fanconi syndrome
- impaired proximal tubular reabsorption of glucose, amino acids, phosphate & bicarbonate
- hyperchloremic acidosis*
- reduced ammonia production
- inability to acidify collecting duct fluid (distal renal tubular acidosis)
- proximal tubular bicarbonate wasting
- tubular or low-molecular weight proteinuria*
- defect is proximal tubular protein reabsorption
- polyuria, isosthenuria*
- hyperkalemia*
- K+ secretory defects
- aldosterone resistance
- salt wasting
- distal tubular damage
- failure of Na+ reabsorption
- reduced GFR*
* common
Laboratory
More general terms
More specific terms
- acute tubular necrosis; tubulorrhexis (ATN)
- hereditary renal tubular defects
- medullary sponge kidney disease
- proximal tubulopathy
- pyelonephritis
- renal tubular acidosis (RTA)
- renal tubular dysgenesis