Preservation of renal function in experimental glomerulonephritis

Abstract

To evaluate the protective effect of dietary phosphorus restriction in an immunologic model of experimental renal disease, we randomized 24 Sprague-Dawley rats with established nephrotoxic serum nephritis into two groups. Group A animals (N = 13) were fed a diet with a normal phosphorus content (0.5% phosphorus), and group B animals (N = 11) received an identical diet low in phosphorus (0.04% phosphorus). Over the ensuing 133 days, group A rats developed progressive renal failure and had a mean serum creatinine concentration of 3.0 +/- 0.5 mg/dl at the time of death or completion of the study. In contrast, group B animals maintained near normal renal function and had a final mean serum creatinine concentration of 0.93 + 0.2 mg/dl (P < 0.001). Survival was markedly improved in group B animals (P < 0.001). Histologic damage was diminished greatly in group B animals by both light and electron microscopy; immunofluorescence was positive in all animals. Group A animals had increased kidney calcium concentration (30 +/- 6 mmoles/kg) when compared to group B animals (18 +/- 1 mmoles/kg) and animals with normal kidneys (13 +/- 1 nmoles/kg, P< 0.001). Conclusion. Dietary restriction of phosphorus retards functional deterioration and reduces histologic damage in experimental immunologic renal disease. The mechanism for this protective effect has not been elucidated.

Association of Disorders in Mineral Metabolism with Progression of Chronic Kidney Disease

“…This finding complements earlier studies that showed a beneficial effect of dietary phosphorus restriction on progression of CKD in experimental animals (5,6,8) and in humans (4,7). The mechanism underlying this association is unclear but may be related to increased nephrocalcinosis, hyperparathyroidism, alterations in cellular energy metabolism, or altered renal hemodynamics (6,13).…”

Risk of Kidney Injury Following Oral Phosphosoda Bowel Preparations

“…[21][22][23] Multiple case reports and controlled human studies 5-7,24 -26 demonstrated that receipt of a standard regimen of OPS (which contains approximately six times the average daily phosphate intake) results in acute rises in serum phosphate. Moreover, data in rat models of CKD (remnant kidney and nephrotoxic serum nephritis) demonstrate that higher levels of dietary phosphate accelerate loss of kidney function 10,11 and that this effect is attenuated by administration of phosphate binders. 12,13 Despite this plausible link, our data do not support an association between receipt of OPS and kidney injury.…”

High phosphorus intake only slightly affects serum minerals, urinary pyridinium crosslinks and renal function in young women

“…Contrarily, animals consuming a low-phosphorus diet had signi®cantly lower serum creatinine concentrations, maintained a normal level of renal function, and showed less accelerated mortality. Restriction of phosphorous in the diet resulted in reduced renal damage and less histological injury in the phosphorus-de®cient mice (Karlinsky et al, 1980). One of the typical indicators of changes in kidney function is urinary microalbumin excretion.…”

“…One of the typical indicators of changes in kidney function is urinary microalbumin excretion. High phosphorus diets induce nephrocalcinosis and depression of kidney function in rats (Matsuzaki et al, 1997(Matsuzaki et al, , 1998Karlinsky et al, 1980). The excretion in urinary microalbumin increased, caused by a defect in the permeability of the renal glomerular basement membrane.…”

“…Karlinsky et al (1980) measured the in¯uence of altered dietary phosphorus on the subsequent development of nephrotoxic serum nephritis in rats. Control animals fed a phosphorus-adequate diet developed a glomerulonephritis characterized by progressive renal failure, elevated concentrations of creatinine in serum, proteinuria and early death (Karlinsky et al, 1980). Contrarily, animals consuming a low-phosphorus diet had signi®cantly lower serum creatinine concentrations, maintained a normal level of renal function, and showed less accelerated mortality.…”