TY - JOUR
T1 - Reversible acute renal failure from gross haematuria due to glomerulonephritis
T2 - Not only in IgA nephropathy and not associated with intratubular obstruction
AU - Fogazzi, G. B.
AU - Imbasciati, E.
AU - Moroni, G.
AU - Scalia, A.
AU - Mihatsch, M. J.
AU - Ponticelli, C.
PY - 1995
Y1 - 1995
N2 - Seven patients with acute renal failure due to gross haematuria caused by glomerulonephritis are described. Gross haematuria lasting 4 40 days led to acute impairment of renal function of variable severity (peak plasma creatinine 1.3–12 mg/dl) and duration. While partial recovery of renal function occurred in all patients within few days, complete remission was observed only some months later. Three patients had IgA nephropathy (2 the primary form and 1 nephritis secondary to Schönlein-Henoch purpura), two patients had acute postinfectious glomerulonephritis, andtwo others had focal necrotizing (pauci-immune) glomerulonephritis. The glomerular changes seen in renal biopsy were not enough to explain per se the renal function impairment. Tubular changes, however, were severe and consisted of tubular necrosis, erythrocyte casts, erythrocyte phagocytosis by tubular cells, accompanied by interstitial damage (oedema, red-cell extravasation, and inflammatory infiltrates). Study of the renal biopsies by immunofluorescence revealed retrodiffusion of Tamm-Horsfall protein into the glomerular Bowmans space, a sign of obstructed tubular flow in any case. It is concluded that acute renal failure due to gross haematuria in glomerulonephritic patients may not occur only in IgA nephropathy, as reported so far, and is not associated with intratubular obstruction.
AB - Seven patients with acute renal failure due to gross haematuria caused by glomerulonephritis are described. Gross haematuria lasting 4 40 days led to acute impairment of renal function of variable severity (peak plasma creatinine 1.3–12 mg/dl) and duration. While partial recovery of renal function occurred in all patients within few days, complete remission was observed only some months later. Three patients had IgA nephropathy (2 the primary form and 1 nephritis secondary to Schönlein-Henoch purpura), two patients had acute postinfectious glomerulonephritis, andtwo others had focal necrotizing (pauci-immune) glomerulonephritis. The glomerular changes seen in renal biopsy were not enough to explain per se the renal function impairment. Tubular changes, however, were severe and consisted of tubular necrosis, erythrocyte casts, erythrocyte phagocytosis by tubular cells, accompanied by interstitial damage (oedema, red-cell extravasation, and inflammatory infiltrates). Study of the renal biopsies by immunofluorescence revealed retrodiffusion of Tamm-Horsfall protein into the glomerular Bowmans space, a sign of obstructed tubular flow in any case. It is concluded that acute renal failure due to gross haematuria in glomerulonephritic patients may not occur only in IgA nephropathy, as reported so far, and is not associated with intratubular obstruction.
KW - Acute renal failure
KW - Acute tubular necrosis
KW - Glomerulonephritis
KW - Gross haematuria
KW - Tamm-Horsfall protein
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U2 - 10.1093/oxfordjournals.ndt.a091185
DO - 10.1093/oxfordjournals.ndt.a091185
M3 - Article
C2 - 7566573
AN - SCOPUS:0029029081
SN - 0931-0509
VL - 10
SP - 624
EP - 629
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
IS - 5
ER -