Alterations in Glomerular Hemodynamics, Parathyroid Hormone Metabolism, and Sys­temic Arterial Blood Pressure



Alterations in Glomerular Hemodynamics in Renal Disease. The nephrons that remain functional in the presence of renal injury are, as noted earlier,not damaged but rather supernormal. Morpholog­ically and functionally, these nephrons are larger and have higher than normal rates of glomerular plasma flow and filtration. The reason for the in­crease in the glomerular plasma flow and the rate of filtration is not known with certainty but is re­lated, at least in part, to the dietary intake of pro­tein. Protein or its peptide fragments cause renal vasodilation, an increase in glomerular plasma flow, and an increase in the glomerular hydro­static pressure. It has been proposed that in renal insufficiency, the superperfusion and hyperfiltra-tion of remaining nephrons, in and of itself, re­sults in glomerulosclerosis and further loss of nephrons. Administration of a lowprotein diet containing proteins of high biological value (pro­teins with a high content of essential amino acids) may result in a reduction in glomerular blood flow, glomerular hydrostatic pressure, and hy-perfiltration and thus slow the progression of the renal disease.

The Role or Parathyroid Hormone. In adapting to a constant intake of phosphate, calcium and phos­phate homeostasis are maintained at the expense of development of hyperparathyroidism. Parathy­roid hormone, however, has several actions that may be detrimental to the kidney. PTH may con­tribute to injury of renal cells by facilitating de­position of calcium in the renal parenchyma or by translocating calcium into the cells and the mi­tochondria. The net effect of parathyroid hormone would be further loss of nephrons and increasing degrees of hyperparathyroidism.

The Role or Blood Pressure. Regardless of the na­ture of the primary renal insult, the codevelop-ment of elevation of the blood pressure results in a significant acceleration in the rate of nephron loss. It has been suggested that aggressive and early treatment of blood pressure elevations, even elevations in the range in which therapy is of questionable value in patients without renal dis­ease, is indicated.

In the evaluation of a patient with progressive renal injury, the clinician must carefully deter­mine if there is evidence of continued activity of primary disease and/or exposure to nephrotoxins. The patient should be carefully evaluated for the existence of secondary forms of renal injury and, if such is present, treated appropriately. If there is neither evidence for active primary disease nor secondary insults, a lowprotein diet containing proteins of high biological value should be insti­tuted. In addition, correction of the phosphatecalciumparathyroid hormone interactions should be considered. Finally, the institution of blood pressure control is of critical therapeutic importance