hypertensive kidney disease hypertensive kidney disease hypertensive kidney disease is a medical condition referring to damage to the kidney due to chronic high blood pressure. it manifests as hypertensive nephrosclerosis (sclerosis referring to the stiffening of renal components). it should be distinguished from renovascular hypertension, which is a form of secondary hypertension, and thus has opposite direction of causation. hypertensive kidney diseaseother nameshypertensive nephrosclerosis (hn or hns), hypertensive kidney disease, hypertensive nephropathy (hn), nephroangiosclerosismicrograph showing renal arterial hyalinosis – pink ring right-of-centre. pas stain.specialtynephrology signs and symptoms signs and symptoms of chronic kidney disease, including loss of appetite, nausea, vomiting, itching, sleepiness or confusion, weight loss, and an unpleasant taste in the mouth, may develop. causes on gross pathology, nephrosclerosis manifests as a fine granular surface. "hypertensive" refers to high blood pressure and "nephropathy" means damage to the kidney; hence this condition is where chronic high blood pressure causes damages to kidney tissue; this includes the small blood vessels, glomeruli, kidney tubules and interstitial tissues. the tissue hardens and thickens which is known as nephrosclerosis. the narrowing of the blood vessels means less blood is going to the tissue and so less oxygen is reaching the tissue resulting in tissue death (ischemia). risk factors for hn include poorly controlled, moderate-to-high blood pressure, older age, other kidney disorders, and afro-caribbean background, whose exact cause is unclear, as it may be due to either genetic susceptibility or poor health management among people of afro-caribbean descent. mechanism in the kidneys, as a result of benign arterial hypertension, hyaline (pink, amorphous, homogeneous material) accumulates in the walls of small arteries and arterioles, producing the thickening of their walls and the narrowing of the arterial openings, a process known as arteriolosclerosis. the resulting inadequate blood flow produces tubular atrophy, interstitial fibrosis, and glomerular alterations (smaller glomeruli with different degrees of hyalinization – from mild to sclerosis of glomeruli) and scarring around the glomeruli (periglomerular fibrosis). in advanced stages, kidney failure will occur. functional nephrons have dilated tubules, often with hyaline casts in the opening of the tubules. additional complications often associated with hypertensive nephropathy include glomerular damage resulting in protein and blood in the urine. hypertensive nephropathy refers to kidney failure that can be attributed to a history of hypertension it is a chronic condition and it is a serious risk factor for the development of end-stage kidney disease (eskd). however, despite the well-known association between hypertension and chronic kidney disease, the underlying mechanism remains unclear. the two proposed mechanisms of hn's pathophysiology both centre around how the glomerulus, a network of dense capillaries that carries out the kidney filtration process, is affected; with one theory identifying glomerular ischemia as the main contributor to hn and the other identifying glomerular hypertension and glomerular hyperfiltration at the centre of hn's pathogenesis. glomerular ischemia high blood pressure in the long term can damage the endothelium, commonly known as the blood vessel lining. this leads to a build-up of plaques and they can be deposited in the renal arteries causing stenosis and ischemic kidney disease. in this situation, the kidney supplied blood by the narrowed renal artery suffers from inadequate blood flow, which in turn causes the size of the kidneys to decrease. other consequences include arterial stiffening, which involves a gradual breakdown of elastic fibers and intima (the innermost layer of a blood vessel) thickening. glomerular hypertension and glomerular hyperfiltration an alternative mechanism of hypertensive nephropathy is prolonged glomerular hypertension and hence glomerular hyperfiltration. these can occur simultaneously but not necessarily. the idea is that hypertension results in sclerosis of the glomeruli which ultimately means reduced kidney function. as a compensatory mechanism, the unaffected nephrons (specifically, the preglomerular arterioles) vasodilate to increase blood flow to the kidney perfusion and increase glomerular filtration across undamaged glomeruli. diagnosis diagnosis of hn is made from clinical history and biochemical investigations. chronic hypertension with progressive kidney disease progresses over a long period of time. damage to the glomeruli allows proteins that are usually too large to pass into the nephron to be filtered. this leads to an elevated concentration of albumin in the urine (albuminuria). this albuminuria usually does not cause symptoms but can be indicative of many kidney disorders. protein in the urine (proteinuria) is best identified from a 24-hour urine collection. bilateral renal artery stenosis should always be considered as a differential diagnosis for the presentation of hn. kidney disease with this etiology can potentially be reversed following vascular intervention. histology in benign nephrosclerosis, the changes occurring are gradual and progressive, however, there can be sufficient kidney reserve capacity to maintain adequate kidney function for many years. the large renal arteries exhibit intimal thickening, medial hypertrophy, duplication of the elastic layer. the changes in small arterioles include hyaline arteriolosclerosis (deposition of hyaline, collagenous material), which causes glomerular collapse (wrinkling and thickening of capillary basement membranes and collapse of capillary lumen) and solidification (glomeruli exhibit sclerosis and increase in mesangial matrix). the degree of scarring correlates with the degree of glomerular filtration deficit. light micrograph showing hypertensive glomerular lesion of hypertensive nephropathy: global glomerular collapse and filling of bowman's space with a lightly staining collagenous material. light micrograph of glomerulus showing secondary segmental sclerosis of hypertensive nephropathy. histopathology of arcuate artery nephrosclerosis, seen as a thickened intima with an onion skin-like architecture. it is presumably a manifestation of hypertensive kidney disease. light micrograph showing signs of hypertensive nephropathy: interstitial fibrosis, tubular atrophy with thickened tubular basement membranes, and fibrous intimal thickening of a small artery (arrow). malignant nephrosclerosis is where hypertensive nephrosclerosis occurs in presence of malignant hypertension (when dbp > 130mmhg). vessels feature intimal thickening, fibrinoid necrosis, red blood cell fragmentation, extravasation, thrombosis. these changes create an exaggerated layered appearance (onion skinning). urine test microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. the majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. in the case of glomerular damage occurring in hn, hematuria can occur as well. definitive diagnosis the definitive diagnosis of hn requires morphological examination. common histological features can be identified in the renal and glomerular vasculature. glomerulosclerosis is often present, either focally or globally, which is characterized by hardening of the vessel walls. also, luminal narrowing of the arteries and arterioles of the kidney system. however, this type of procedure is likely to be preceded by a provisional diagnosis based on laboratory investigations. future diagnostic approaches increasing access to, and use of, genome profiling may provide opportunity for diagnosis based on presentation and genetic risk factors, by identifying apol1 gene variants on chromosome 22. management