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Mackensen-Haen S, Eissele R, Bohle A. Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis. Lab Invest. 1988;59(2):239-44
Mackensen-Haen, S., Eissele, R., & Bohle, A. (1988). Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis. Laboratory investigation; a journal of technical methods and pathology, 59(2), 239-44.
Mackensen-Haen, S, et al. "Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis." Laboratory investigation; a journal of technical methods and pathology vol. 59,2 (1988): 239-44.
Mackensen-Haen S, Eissele R, Bohle A. Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis. Lab Invest. 1988 Aug;59(2):239-44. PMID: 3404975.
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Lab Invest. 1988 Aug;59(2):239-44.

Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis.

Laboratory investigation; a journal of technical methods and pathology

S Mackensen-Haen, R Eissele, A Bohle

Affiliations

  1. Institute for Pathology, University of Tuebingen, Federal Republic of Germany.

PMID: 3404975

Abstract

The following findings were obtained in a comparative morphometric and clinical study of 130 adult men and women with immunologically confirmed IgA nephritis: (a) IgA nephritis develops in varying frequency as minimal proliferating intercapillary glomerulonephritis, low-grade mesangioproliferative glomerulonephritis, moderate to severe mesangioproliferative glomerulonephritis, or variously severe mesangioproliferative glomerulonephritis with signs of focal accentuation. (b) Tubular epithelial surface area and interstitial width in 62 of 130 cases of IgA nephritis was the same as in normal kidneys. IgA nephritis was complicated in 33 cases by interstitial cortical fibrosis, in 23 cases by acute renal failure, and in 12 cases by acute renal failure and interstitial fibrosis. (c) In IgA nephritis with acute renal failure, the tubular epithelium (only proximal tubular epithelium was measured) was significantly swollen. In IgA nephritis with interstitial fibrosis, the epithelial surface area of the proximal tubules was significantly smaller than the normal surface area. In IgA nephritis with acute renal failure (ARF) and interstitial fibrosis, tubular swelling was less severe than in ARF. Proximal tubular epithelial surface area, however, was significantly larger than the normal surface area. (d) In IgA nephritis, like in other inflammatory and noninflammatory glomerular diseases, a significant positive correlation existed between width of the cortical interstitium and height of serum creatinine level. Moreover, in IgA nephritis, significantly negative correlation existed between width of the cortical interstitium and C creatinine. (e) In IgA nephritis, significant negative correlations existed between C creatinine and age. (f) In IgA nephritis, a significant correlation existed between proximal tubular epithelial surface area and serum creatinine level and a significant negative correlation, between C creatinine and proximal tubular epithelial surface area, when ARF cases were excluded from the total group of IgA nephritis. (All correlations are closer when the cases with accompanying ARF are eliminated.) The discrepancy between the findings of Bennett et al. (Bennett WM, Walker RG, Kincaid-Smith P: Lab Invest 47:330, 1982) and ours is clarified when it is presumed that the group of patients investigated by Bennett et al. (N = 85) included just as many ARF cases as our material. Consequently, there is no reason to correct our interpretation of the influence of tubulointerstitial changes on glomerular function.

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