Kidney disease hypertensive nephropathy

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."... 

Diabetes is the most frequent cause of end-stage renal disease. Hypertension, which is common among patients with type 2 diabetes, accelerates the development and progression of renal disease. Early and tight blood pressure control in diabetic patients, preferably with antihypertensive agents that have proven reno-protective properties, is therefore essential to minimize loss of kidney function. Several controlled clinical trials have investigated and proved the beneficial effects of ARBs on type 2 diabetic nephropathy [10-14]. 

ACE-inhibitors may be considered as first-choice therapy in patients with all forms of primary hypertension, but they are preferred in hypertension associated with heart failure, reduced systolic left ventricular ejection fraction or diabetic nephropathy, previous MI or stroke, chronic kidney disease and patients with high coronary disease risk, based on the compelling evidence of the efficacy of these drugs in such patient populations [8]. 

Lead nephropathy does not account for renal failure in all hypertensives with kidney disease any more than it accounts for renal failure in all gout patients with kidney disease. The heavy metal may, however, contribute to the association of gout with hypertension, as well as to the variable incidence of renal failure in each of these conditions. 

End-stage renal disease is treated with dialysis and kidney transplantation. Hypertension and cardiovascular diseases affect the Balkan nephropathy patients less frequently, so they tolerate hemodialysis rather well compared to patients with other renal diseases. The Balkan nephropathy patients on long-term hemodialysis frequenfly develop upper urothelial or urinary bladder carcinoma. 

Proteinuria is a common finding in patients with kidney disease, and the use of a dipstick assay is an important screening test in any patient suspected of having renal disease. Among patients with suspected or proven CKD, including reflux nephropathy and early glomerulonephritis, and those with hypertension or previously detected asymptomatic hematuria, annual urinalysis for proteinuria is accepted as a useful way of identifying patients at risk of... 

It is not known whether these changes are the result of a normal aging process (i.e., involutional) or the result of the interplay of pathology and age. Cumulative exposure to common causes of chronic kidney disease (CKD), such as (1) atherosclerosis, (2) hypertension, (3) heart failure, (4) diabetes,(5) obstructive nephropathy, (5) infection, (6) immune insult, (7) nephrotoxins such as lead, and (8) dietary protein increases with age and it is difficult to separate these effects from those of healthy aging. The decline in GFR with increasing age may be largely attributable to hypertension, atherosclerosis, or heart failure. In the absence of these or other identifiable causes of kidney disease, many older subjects have stable GFR over time. 

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. 

Hypertensive crises, renovascuiar hypertension, neonatai and chiidhood hypertension, stroke prevention, migraine prophyiaxis, nondiabetic nephropathy, chronic kidney disease, diagnosis of scieroderma renai crisis, and Bartter s syndrome (32,33)... 

Lead nephropathy has also been complicated by the toxicological interactions of chronic kidney disease with adverse cardiovascular effects such as hypertension. Hypertension, as noted in this chapter, is a risk factor for Pb-associated and non-Pb-associated kidney disease, while mechanisms for inducing hypertension include the participation of kidney biochemistry and physiology via, for example, the renin—angiotensin pathway. 

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. 

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

In type 1 diabetes, diabetic nephropathy follows a predictable course from onset of diabetes to the onset of microalbuminuria to frank nephropathy to end-stage renal disease or death. Microalbuminuria (a tiny amount of protein in the urine) develops 10-14 years after onset of diabetes. Without treatment, clinical nephropathy follows within 5 years, and severe renal impairment leading to end-stage renal failure develops approximately 5 years later. Hypertension develops in association with microalbuminuria and progresses with diabetic nephropathy, further damaging the kidneys. Once end-stage renal disease (ESRD) is reached, the toxins in the body can no longer be cleared by the kidneys and, unless treated by dialysis, can build up to fatal levels. 

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