Nephrosclerosis, hypertensive

The glomerulus is situated between two sets of resistance vessels, the afferent and efferent arterioles, thus preventing transmission of this pressure to the glomerulus. This compensatory mechanism may be one explanation for the relatively low incidence of hypertensive nephrosclerosis (1.5-4%) among patients with mile to moderate hypertension. In the intrarenal vasculature, angiotensin receptors are found in greater density in the efferent... 

Angiotensin II is an octapeptide, which was initially described as a potent vasoconstrictor agent. However, its functions have since been expanded to include regulation of cell growth, inflammation, electrolyte and water balance, hormone secretion, sympathetic nervous system activity, differentiation, and apoptosis. The discovery that it is produced both systemically and locally was instrumental in establishing a pivotal role for the peptide in several disease states, including hypertension, coronary heart disease, myocarditis, congestive heart failure, atherosclerosis, and nephrosclerosis. 

Intra-renal arteriolar changes indistinguishable from nephrosclerosis are found, often in the absence of clinical hypertension [4]. The appearance of arteriolar nephrosclerosis before hypertension develops and the relatively short duration of hypertension before renal failure supervenes suggest that the initial renal injury from lead may be in the microvascular endothelium... 

Freedman BI, Iskander SS, Appel RG. The link between hypertension and nephrosclerosis. Am J Kidney Dis 1995 25 207-21. 

Vascular nephropathy in prolonged hypertension is associated with a degeneration of the arterial walls. The resulting nephrosclerosis is due to the loss of functional glomeruli, leading to diminished renal function. 

Coronary artery disease, hypertension, hypercholesterolemia Vascular changes, cerebrovascular disease, retinal microaneurysms Nephrosclerosis, renal disease Weakness, paresthesias, peripheral neuritis, cranial nerve injury, pain, footdrop, abnormal gait, tremor, choreiform movements, optic neuritis, polyneuropathy, parkinsonism, headache, electroencephalogram changes, retrobulbar neuritis... 

Solvents have been implicated as inducers of glomerulonephritis [72], while the association between chronic interstitial nephritis and analgesic abuse is acknowledged [73] and the association between hypertensive renal disease (nephrosclerosis) and lead nephropathy continues to be explored [74, 75]. According... 

The risk of ACE inhibitor-induced renal impairment in patients with or without renovascular disease can be potentiated by diuretics. " In an analysis of 74 patients who had been treated with captopril or lisinopril, reversible acute renal failure was more coimnon in those who were also treated with a diuretic (furosemide and/or hydrochlorothiazide) than those who were not (11 of 33 patients compared with 1 of 41 patients). Similarly, in a prescription-event monitoring study, enalapril was associated with raised creatinine or urea in 75 patients and it was thought to have contributed to the deterioration in renal function and subsequent deaths in 10 of these patients. However, 9 of these 10 were also receiving loop or thiazide diuretics, sometimes in high doses. Retrospective analysis of a controlled study in patients with hypertensive nephrosclerosis identified 8 of 34 patients who developed reversible renal impairment when treated with enalapril and various other antihypertensives including a diuretic (furosemide or hydrochlorothiazide). In contrast, 23 patients treated with placebo and various other antihypertensives did not develop renal impairment. Subsequently, enalapril was tolerated by 7 of the 8 patients without deterioration in renal function and 6 of these patients later received diuretics. One patient was again treated with enalapril with recurrence of renal impairment, but discontinuation of the diuretics (furosemide, hydrochlorothiazide, and triamterene) led to an improvement in renal function despite the continuation of enalapril. ... 

The types of tumour which cause a permanent hypertension, and which may be preceded by a stage of paroxysmal hypertension, frequently simulate essential hypertension or, in the course of a prolonged development, a malignant nephrosclerosis. Alterations in the vascularity of the retina, proteinuria, and an increasing reduction of the renal functions, are the consequences. The relatively frequent occurrence of such symptoms make it necessary to take the phaeochromocytoma into consideration as a possible cause of every hypertension of long duration. It may also be the cause of a diabetes resistance to insulin and accompanied by hypertension, or the simultaneous occurrence of hypertension and an increased basal metabolic rate together with a normal radio-iodine absorption by the thyroid gland. The illness is very improbable in the obese. 

Individuals with hypertension and elevated Pb exposures appear to be at increased risk for Pb nephropathy (hypertensive nephrosclerosis), although the question of direction of any association remains problematic, in that hypertension aggravates the severity and course of kidney disease while Pb exposure has a hypertensive effect in the human cardiovascular system. 

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