Renal Dysfunctions in Glomerulonephropathy with Rapidly Declined Renal Failure

Abstract

Eight patients aged between 5 and 26 years developed rapid deterioration of renal function and became oliguric/anuric with duration ranging from 1 to 21 days. The initial functional assessment revealed severe degree of glomerular, tubular, and vascular dysfunctions. The magnitude of renal dysfunction was quantified and expressed in terms of a clinical score. The degree of glomerular and tubular dysfunctions were inversely proportional to the renal plasma flow and peritubular capillary blood flow (PTCB), respectively. Similar findings have been observed in a variety of severe glomerulonephropathies. In this aspect, it is likely that the reduction of peritubular capillary blood flow and tubulointerstitial disease are interrelated. Further evidence to support the primary role of reduction of PTCB in inducing tubulointerstitial disease is provided by the following: (a) Reduction of PTCB is documented in mesangial proliferative nephrosis with steroid resistance prior to the detection of tubulointerstitial disease. (b) Ischemic insult can induce tubulointerstitial disease in experimental setting of renal artery occlusion in animal, (c) Improved tubular function can be achieved following the increase in PTCB with the enhanced renal perfusion therapy.

Peritubular Capillary Flow Determines Tubulointerstitial Disease in Idiopathic Nephrotic Syndrome

“…On the contrary, a therapeutic approach aiming to improve the renal perfusion with a variety of drugs would likely be able to retard, improve or even prevent the renal disease progression. The result of such therapeutic approach with so called``enhanced renal perfusion formula which has been launched to treat a variety of nephrotic patients, appears to be superior to the conventional regimen [8][9][10][11][12][13][14][15] Figure 1. Illustrates the correlation between peritubular capillary¯ow and tubulointerstitial ®brosis.…”

Hemodynamic Correction and Early Detection of Tubulointerstitial Fibrosis Prevent Disease Progression in Chronic Kidney Disease

“…With respect to the former, an early detection of TIF can be achieved by using a determination of fractional excretion of magnesium (FE Mg), which correlates directly with TIF since it reflects the tubular reabsorptive capability and intratubular wastage of magnesium in association with tubulointerstitial injury. [1] FE Mg is normal in minimal change disease or in acute glomerulonephritis with intact tubulointerstitial structure and is consistently elevated in conditions associated with TIF namely FSGS, IgM nephropathy with TIF, IgA N, reflux nephropathy, severe lupus nephritis, chronic glomerulonephritis and diabetic nephropathy [2] (unpublished data).…”