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. File:Histopathology of<unk>  glomerular lesion of<unk>  nephropathy.Light micrograph showing<unk>  glomerular lesion of<unk>  nephropathy: global glomerular collapse and filling of Bowman’s space with a lightly staining collagenous material. File:Histopathology of secondary segmental glomerular sclerosis of<unk>  nephropathy.Light micrograph of glomerulus showing secondary segmental sclerosis of<unk>  nephropathy. File:Histopathology of arcuate artery nephrosclerosis, annotated.Histopathology of arcuate artery nephrosclerosis, seen as a thickened intima with an onion skin-like architecture. It is presumably a manifestation of<unk> . File:Histopathology of renal interstitial fibrosis of<unk>  nephropathy.Light micrograph showing signs of<unk>  nephropathy: interstitial fibrosis, tubular atrophy with thickened tubular basement membranes, and fibrous intimal thickening of a small artery (arrow). Malignant nephrosclerosis is where<unk>  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.
Hypertensive kidney disease
Renovascular hypertension
Diabetic nephropathy
Lupus nephritis
Benign nephrosclerosis
Polycystic kidney disease
Analgesic nephropathy
Cystic kidney disease