Tamm-Horsfall Protein Accumulation in Glomeruli during Acetazolamide-Induced Acute Renal Failure

Abstract

A patient with ocular hypertension was treated with acetazolamide. Acute renal failure developed rapidly and renal biopsy showed mild tubular lesions and crystal formation in a tubular lumen. By immunofluorescence studies with a monoclonal antibody, Tamm-Horsfall protein, normally absent from the proximal segments of the nephron, was detected in most glomeruli. This strongly suggests that tubular obstruction plays a major part in some cases of acetazolamide-induced acute renal failure.

Reversible acute renal failure from gross haematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction

“…In spite of the fact that there were intratubular casts in all our biopsies, we were unable to observe retrodiffusion of THp into the glomerular Bowman's space, which has been observed in several other conditions such as obstructive uropathy [13][14][15], myeloma cast nephropathy [16,17], acute renal failure after acetazolamide intake [18], or in glomerular diseases associated with tubulointerstitial damage [12]. Since the retrodiffusion of THp into Bowman's space is considered to be a sign of intratubular obstruction, its absence in our patients suggests that this mechanism was not involved in the acute renal failure from gross haematuria.…”

“…A sign of intratubular obstruction was considered the presence of THp within Bowman's capsule [12][13][14][15][16][17][18]. Stain intensity was scored from 0 to + + +.…”

Acyclovir-Induced Acute Tubulo-Interstitial Nephritis

“…The significance of Tamm-Horsfall protein spillage in the development of interstitial inflammatory reaction is not clear. In a case of acetazolamide-induced acute renal failure, but without interstitial inflammation, the detection of Tamm-Horsfall protein in the glomeruli by immunofluorescence techniques has suggested that tubular obstruction by cellular debris and crystals plays a major role in the pathogenesis of acetazolamide-induced acute renal fail ure [11]. No crystal has been seen in the renal biopsies of our cases or the one case reported in the literature [6] to support crystal nephropathy, an idea based on the exami nation of animal renal tissue a few minutes after high bolus doses [5] which differs markedly from the clinical situation using slow infusions.…”

Systemic Side Effects of Glaucoma Medications

“…Thus, CAI agents cause a metabolic acidosis and will reduce total body sodium and potassium. 74 Even though patients with end-stage renal disease are functionally anephric, preexisting renal failure associated acidosis may be worsened by acetazolamide as a result of inhibition of extrarenal buffers in bone. First, despite persistent CA inhibition, the loss of plasma bicarbonate plateaus.…”