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Hypertension prevalence rates in most urbanized areas of Africa range from 20–30%, with a recent systematic review reporting 16.2% for sub-Saharan Africa. These rates are lower than those in the West but the age standardized rates are higher than in other regions of the world. The attendant morbidity and mortality are disproportionately high. For example, failure of nocturnal dipping and microalbuminuria, predictive of vascular disease, occur relatively early in the course of hypertension and predispose to early vascular disease. Multiple target organ damage occurs in a large proportion, up to 50%, of newly-diagnosed hypertensives and this is more marked when kidney disease is present.

By most accounts, hypertension ranks second to glomerulonephritis as the commonest causes of ESRD in Africa, with diabetes rates rapidly increasing in the last 3 decades. The contribution of hypertension to the causation of ESRD is of the order of 25–35%, lower than in US Blacks, with the odds of developing ESRD increasing with increasing BP levels. Hypertension and renal disease often coexist, and nephrosclerosis can often be distinguished from primary renal disease by employing a set of parameters including age of onset of hypertension and renal disease, other clinical signs and level of proteinuria. In other cases, this could be difficult especially where investigative facilities are limited, a common situation in most parts of Africa. Indeed, up to 35% of cases of presumed nephrosclerosis may actually have primary renal disease, which can only be revealed after more extensive investigations.

There is genetic heterogeneity in the susceptibility to kidney disease in hypertension associated with APOL 1 gene risk variants. In addition, environmental factors, including salt consumption, contribute to the propensity for elevated BP and vascular disease. The association with APOL 1 gene variants also raises the probability of an underlying glomerulopathy in kidneys which subsequently develop nephrosclerosis, sometimes despite adequate BP control. Glomerular hypertrophy appears to be the major pathogenetic path leading to nephrosclerosis, with loss of autoregulation initiating events which lead to hyperfiltration, glomerular hypertrophy and glomerulosclerosis. Glomerular and interstitial changes occur early and there are reports of proteinuria correlating with the BP. Albuminuria and reduced eGFR have been found in 3–15% and up to 60% respectively, of newly diagnosed hypertensives.

Benign and malignant nephrosclerosis are recognized. Even with benign nephrosclerosis, the renal disease and outcome are worse than in other groups. There is a disproportionate occurrence of malignant hypertension, probably related to inadequate BP control and psychosocial stress, with resulting poor renal function and outcomes which appear to dominate the clinical picture. Renal involvement occurs in virtually all cases of malignant hypertension with proteinuria and haematuria occurring in 100% of cases in some reports. Mucoid intimal proliferation in the interlobular artery and afferent arteriole, occurs in 100% of cases, and fibrinoid necrosis in these sites and the glomerulus, occurs in over 80% of cases; these constitute the characteristic vascular lesions.

In treatment, BP control is paramount in slowing the progression of kidney disease and reducing overall cardiovascular risk. Recommended drugs include diuretics, angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB) and calcium antagonists (CA). ACEIs and ARBs, increasingly used, are particularly effective in the additional reduction of proteinuria although BP reduction by other means may lead to more modest reductions in proteinuria. The use of dihydropyridine CA may carry some risk in this regard and the combination of ARB or ACEI and CA is gaining popularity despite the cost. In many parts of Africa, methyldopa is still widely used. Renal function often worsens, transiently, following reduction of BP in malignant hypertension, especially with severe renal disease, leading to early and temporary need for dialysis. Target BP of 140/90 mmHg is seldom achieved in the majority of patients with hypertensive renal disease in Africa, even though there are advocates for a lower target.

Additional measures include control of glycaemia, lipidaemia, dietary protein restriction and avoidance of nephrotoxic agents, a particular problem in most parts of Africa. With ESRD, dialysis, usually haemodialysis, is given and there is growing use of renal transplantation. The availability of renal replacement therapy is however limited and only a small percentage of patients actually receive it. Reports have shown that under 20% of patients who start dialysis are able to sustain it for more than 3 months. Long term prognosis is influenced by degree of control of BP and availability of renal replacement therapy.

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