高血压英文ppt精品课件renal disorder in systemic

Renal disorder in systemic disease A huge variety of systemic conditions can affect the function of the kidneys, from acute illnesses to drugs and more insidious illnesses. Diabetic nephropathy Hypertensive nephropathy/nephrosclerosis Vasculitides Sickle cell disease Diabetic nephropathy Definition: A microvascular complication of diabetes marked by albuminuria and a deteriorating course from normal renal function to ESRD. Diabetic nephropathy is the commonest cause of end stage renal failure (ESRF) in the developed world (about 3040% of cases of ESRF). Incidence rising in line with diabetes. It is more common as a complication of type 1 diabetes mellitus but also affects a significant proportion of type 2 patients It usually affects patients who have had diabetes for 10 years, with peak incidence of 3% per year in those who have had diabetes for 1020 years The diabetic kidney The kidney may be damaged by diabetes in three main ways: glomerular damage ischaemia resulting from hypertrophy of afferent and efferent arterioles ascending infection. Pathology Expansion of mesangial matrix with diffuse and nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) Thickening of glomerular and tubular BM Arteriosclerosis and hyalinosis of afferent and efferent arterioles Tubulointerstitial fibrosis Signs and Symptoms Approximately 25% to 40% of patients with DM 1 ultimately develop diabetic nephropathy (DN), which progresses through five predictable stages. Stage 1 (very early diabetes) Increased demand upon the kidneys is indicated by an above-normal glomerular filtration rate (GFR). Hyperglycemia leads to increased kidney filtration (see later) This is due to osmotic load and to toxic effects of high sugar levels on kidney cells Increased Glomerular Filtration Rate (GFR) with enlarged kidneys (developing diabetes)Stage 2 Clinically silent phase with continued hyper filtration and hypertrophy The GFR remains elevated or has returned to normal, but glomerular damage has progressed to significant microalbuminuria (small but above-normal level of the protein albumin in the urine). Significant microalbuminuria will progress to end- stage renal disease (ESRD). Therefore, all diabetes patients should be screened for microalbuminuria on a routine basis. (overt, or dipstick-positive diabetes)Stage 3 Glomerular damage has progressed to clinical albuminuria. Basement membrane thickening due to AGEP The urine is “dipstick positive,“ containing more than 300 mg of albumin in a 24-hour period. Hypertension (high blood pressure) typically develops during stage 3. (late-stage diabetes)Stage 4 Glomerular damage continues, with increasing amounts of protein albumin in the urine. The kidneys filtering ability has begun to decline steadily, and blood urea nitrogen (BUN) and creatinine (Cr) has begun to increase. The glomerular filtration rate (GFR) decreases about 10% annually. Almost all patients have hypertension at stage 4. (end-stage renal disease, ESRD)Stage 5 GFR has fallen to 10 ml/min and renal replacement therapy (i.e., haemodialysis, peritoneal dialysis, kidney transplantation) is needed. Diagnosis The urine of all diabetic patients should be checked regularly for the presence of protein. detected by measuring the albumin/creatinine ratio on a spot urine sample Clinical suspicion of a non-diabetic cause of nephropathy may be provoked by an atypical history, the absence of diabetic retinopathy (usually but not invariably present with diabetic nephropathy) and the presence of red cell casts in the urine. Renal biopsy should be considered in such cases, but in practice is rarely necessary or helpful. The risk of intravenous urography is increased in diabetes, especially if patients are allowed to become dehydrated pri or to the procedure, and a renal ultrasound is preferable but not so informative. A 24-hour urine collection is performed to quantify protein loss and to measure creatinine clearance, and regular measurement is made of the plasma creatinine level. Investigation Urine microscopy Culture Serum protein electrophoresis Serum calcium Serum urate ESR Antinuclear factor. :Management of diabetic nephropathy Tight glycaemic control, ideally achieved through combination of dietary modification, pharmacotherapy (including insulin regimen) and regular physical activity. Tight BP control of at least 130/80 through the use of ACE inhibitors/Angiotensin-2 receptor antagonists diuretics/beta-blockers. ACE inhibitors are of benefit in normotensive diabetics with microalbuminuria. Optimisation of other vascular risk factors through use of aspirin and statins (vastly increased cardiovascular risk caused by diabetic nephropathy). Renal replacement therapy (including transplantation) in those with established kidney disease. Hypertensive nephropathy/nephrosclerosis Renal disease can cause hypertension, but sustained hypertension damages the vasculature of the kidneys. This is particularly so in cases of accelerated or malignant hypertension. Hypertensive nephropathy accounts for about a quarter of all patients with ESRF. Hypertension causes a pathology known as nephrosclerosis due to ischaemia affecting the glomeruli, and hyperfiltration causing intraglomerular hypertension. Hypertension also increases the risk of renal failure through the effects of: Cholesterol embolisation to the kidneys The presence of renal artery stenosis (particularly if bilateral) Most patients present with significant hypertension and/or its complications (e.g. cardiac failure, MI, stroke) or biochemical/clinical evidence of renal failure. There has usually been a history of hypertension for about 10 years, but some patients will present without having had any previous evidence of hypertension. Management Management is through use of a range of anti-hypertensive agents, particularly ACE inhibitors/angiotensin-2 antagonists and diuretics, but other agents are also used. The cohort of patients with hypertensive nephropathy are at risk of bilateral renal artery stenosis which may preclude the use of ACE inhibitors due to worsening of renal function. Renal parameters must be monitored very closely after introduction/dose-alteration of an anti-hypertensive agent. Close attention to modification of other cardiovascular risk factors and renal replacement therapy are also useful in improving long-term outlook. Revascularisation of the kidneys (via angioplasty/stenting) may be considered in cases of bilateral renal artery stenosis where there is evidence from captopril renography that it is significantly affecting renal function. Vasculitides Primary systemic vasculitides may cause renal dysfunction through their ability to cause a focal necrotising glomerulonephritis. They usually cause a pattern of renal disease known as rapidly progressive glomerulonephritis (RPGN). Vasculitides that affect the renal vasculature tend to be those that affect medium-sized arteries. : that tend to cause renal impairmentVasculitides Wegeners granulomatosis Microscopic polyangiitis Churg-Strauss syndrome Polyarteritis nodosa Sickle cell disease Many children with sickle cell disease develop hyposthenuria, an inability to form concentrated urine, that may cause nocturnal enuresis and polyuria. Acute severe haematuria may occur due to renal papillary necrosis or sickling within the substance of the kidney and is usually treated with DDAVP/epsilon-aminocaproic acid. A post-mortem series of adult patients with sickle cell disease found that renal failure was the cause of death in about 20% of cases. The disease causes a glomerulopathy with proteinuria and progressive renal insufficiency, leading t