Nephropathy hypertensive

All hypotensive drugs lower systemic BP but, due to the specific characteristics of the glomerular capillary system, different agents may affect glomerular hemodynamics in different ways. This could be of major importance. During antihyper-tensive therapy, systemic BP may be reduced but glomerular pressure may be elevated. This may explain why the incidence of some cardiovascular complications such as stroke, has decreased, whereas the incidence of hypertensive nephropathy has remained high. 

Until late in the course of hypertensive nephropathy, renal damage is asymptomatic and laboratory findings are subtle. The first objective sign of renal involvement is a small increase in the amount of albumin in the urine. 

Exposure to lead in adults has been associated with hypertension, nephropathy, decreased hearing acuity, anemia, peripheral neuropathy, and encephalopathy. Onset of symptoms may be slow with chronic exposure. Anemia, common in chronically exposed adults and children, tends to be more severe in children. The life span of red blood cells decreases when lead concentrations in blood increase. In the past, the morphology of various blood cells was used to diagnose lead poisoning. Zero content is allowed in food (Food and Drug Administration). 

Diseases of the kidney that are discussed in this section include (1) the uremic syndrome, (2) chronic kidney disease, (3) end-stage renal disease, (4) diabetic nephropathy, (5) hypertensive nephropathy, (6) glomerular diseases, (7) interstitial nephritis, (8) polycystic Iddney disease, (9) polycystic kidney disease, (10) toxic nephropathy, (11) obstructive uropathy, (12) tubular diseases, (13) renal calculi, and (14) cystinuria. In addition, this section also includes discussions on (1) prostaglandins and NS AIDS in kidney disease, (2) monoclonal light chains and kidney disease, and (3) urinary osmolality. 

A 67-year-old man with end-stage renal disease secondary to hypertensive nephropathy developed a herpes zoster infection and was given oral valaciclovir 1 g/day. After 5 days, he complained of hallucinations. Valaciclovir was withdrawn and peritoneal diatysis was continued. The serum aciclovir concentration on admission was 20 mg/1 and fell to 0.7 mg/1 by day 7, when his symptoms had completely resolved. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

In the treatment of hypertension, ACE inhibitors are as effective as diuretics, (3-adrenoceptor antagonists, or calcium channel blockers in lowering blood pressure. However, increased survival rates have only been demonstrated for diuretics and (3-adrenoceptor antagonists. ACE inhibitors are approved for monotherapy as well as for combinational regimes. ACE inhibitors are the dtugs of choice for the treatment of hypertension with renal diseases, particularly diabetic nephropathy, because they prevent the progression of renal failure and improve proteinuria more efficiently than the other diugs. 

Boscolo P, Galli G, Iannaccone A, et al. 1981. Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy. Life Sci 28 175-184. 

WedeenRP. 1988. Bone lead, hypertension, and lead nephropathy. Environ Health Perspect 78 57-60. 

Most progressive nephropathies share a final common pathway to irreversible renal parenchymal damage and ESRD (Fig. 76-1). Key pathway elements are loss of nephron mass, glomerular capillary hypertension, and proteinuria. 

The ACE gene encodes two isozymes (somatic ACE isozyme and germinal ACE isozyme). ACE is a membrane-bound enzyme on the surface of vascular endothelial cells that also circulates in plasma and shows great individual variability determined by an I/D polymorphism in intron 16 of the ACE gene (ACE-I/D polymorphism). More than 160 ACE polymorphisms have been reported, 34 of which are located in coding regions, and 18 are missense mutations (606). ACE-related polymorphic variants have been associated with hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic renal failure in IgA nephropathy, Henoch-Schonlein purpura nephritis, mechanical efficiency of skeletal muscle, intracranial aneurysms, susceptibility to myocardial infarction, diabetic nephropathy, AD, and longevity (12,606,607). 

Nephropathy has been associated with chronic lead poisoning. " A study of two large cohorts of heavily exposed lead workers followed through 1980 demonstrated a nearly threefold excess of deaths attributed to chronic nephritis or other hypertensive disease, primarily kidney disease. Most of the excess deaths occurred before 1970, among men who began work before 1946, suggesting that current lower levels of exposure may reduce the risk. Experimental animal studies suggest there may be a threshold for lead nephrotoxicity, and in workers, nephropathy occurred only in those with blood levels over 62p,g/dl for up to 12 years."... 

Nephropathy in type 2 diabetes (iosartan and /nbesarfanj.Treatment of diabetic nephropathy with an elevated serum creatinine and proteinuria (urinary albumin to creatinine ratio greater than or equal to 300 mg/g) in patients with type 2 diabetes and a history of hypertension. 

Older patients have predominantly Type 2 diabetes mellitus, which shares with Type 1 the risk for retinopathy, nephropathy and neuropathy, but carries a greater risk for macrovascular complications such as coronary artery disease, stroke and peripheral vascular disease. Many such patients have associated obesity, hypertension and hyperlipidemia, compounding the risk of cardiovascular disease. The goals of treatment of DM in the elderly are to decrease symptoms related to hyperglycaemia and to prevent long-term complications. Treatment of type 2 DM can improve prognosis. In the UKPDS trial, sulphonylureas, insulin, and metformin were all associated with a reduction in diabetes-related... 

Interestingly, suppressing the Renin-Angioten-sin-Aldosteron System (RAAS) using ACE-I or ARB will reduce the risk for HF in patient with diabetes, even if they do not have hypertension. These drugs have been shown to be beneficial for patients with diabetic nephropathy, and via the same mechanism to also reduce the HF risk. There is abundant support in the literature for the usefulness of RAAS suppression in diabetes combined with cardiovascular disease. 

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