basics Flashcards
Azotemia is an elevation of blood urea nitrogen and creatinine levels and usually reflects a decreased GFR.
prerenal azotemia andhypoperfusion of the kidneys (usually due to reduced extracellular fluid volume). This decreases GFR in the absence of renal parenchymal damage and is usually reversible if the hypoperfusion is corrected in time
Postrenal azotemia results when urine outflow is obstructed.
azotemia gives rise to clinical manifestations and systemic biochemical abnormalities, it is termed uremia. Uremia is characterized by other abnormalities too.
Nephrotic syndrome:
Proteinuria, with daily protein loss (3.5 g )
• Hypoalbuminemia, with plasma albumin level< 3 g/dL
• Generalized edema Hyperlipidemia and lipiduria
derangement of GBM, permeability to plasma proteins
proteinuria, serum albumin is decr, giving rise to hypoalbuminemia and a drop in plasma colloid osmotic pressure, which leads to edema,leakage of fluid from the blood into extravascular spaces. decrease in intravascular volume and renal blood flow triggers increased release of renin from renal juxtaglomerular cells. Renin in turn stimulates the RAAS, which promotes the retention of salt and water by the kidney. dec natriuretic factors. continuing proteinuria, salt and water retention further inc the edema and if unchecked may lead to the development of generalized edema anasarca).
hypoalbuminemia triggers increased synthesis of lipoproteins in the liver, or massive proteinuria causes loss of an inhibitor of their synthesis. There also is abnormal transport of circulating lipid particles and impairment of peripheral breakdown of lipoproteins
focal segmental glomerulosclerosis(adults) and minimal-change disease(kids).
nephritic syndrome is characterized by:
• Hematuria (red cells and red cell casts in urine
• Proteinuria (usually in the subnephrotic range) with or without edema
Azotemia
HTN
nephritic syndrome usually has an acute onset and is caused by inflammatory lesions of glomeruli.
The lesion that nephritic syndrome have in common proliferation of the cells within the glomeruli, often accompanied by an infiltrate of leukocytes. The inflammatory reaction injures the capillary walls, permitting blood to pass into the urine. and induces hemodynamic changes that lead to a reduction in the GFR. The reduced GFR is manifested clinically by oliguria, fluid retention, and azotemia. Hypertension is a result of both the fluid retention and augmented renin release from the ischemic kidney
Asymptomatic hematuria or nonnephrotic proteinuria or a combination of the two is the typical clinical presentation of IgA nephropathy, Alport syndrome, or mild forms or early presentations of other glomerular diseases
The lesion that nephritic syndrome have in common proliferation of the cells within the glomeruli, often accompanied by an infiltrate of leukocytes. The inflammatory reaction injures the capillary walls, permitting blood to pass into the urine. and induces hemodynamic changes that lead to a reduction in the GFR. The reduced GFR is manifested clinically by oliguria, fluid retention, and azotemia. Hypertension is a result of both the fluid retention and augmented renin release from the ischemic kidney
Asymptomatic hematuria or nonnephrotic proteinuria or a combination of the two is the typical clinical presentation of IgA nephropathy, Alport syndrome, or mild forms or early presentations of other glomerular diseases
Rapidly progressive glomerulonephritis (RPGN) results in rapid loss of renal function in a few days or weeks, typically in the setting of nephritic syndrome.
The characteristic histologic finding associated with RPGN is the presence of crescents (crescentic GN). Rapidly progressive glomerulonephritis is a clinical syndrome and not a specific etiologic form of GN. If untreated, it leads to death from renal failure within a period of weeks to months
AKI
abrupt onset of renal dysfunction characterized by an acute increase in serum creatinine often associated with oliguria or anuria (decreased or no urine flow). It can result from glomerular injury (such as rapidly progressive GN), interstitial injury, vascular injury (such as thrombotic microangiopathy), or acute tubular epithelial cell injury.
CKD
results from progressive scarring in the kidney of any cause.
It is characterized by various metabolic and electrolyte abnormalities such as hyperphosphatemia, dyslipidemia, and metabolic acidosis. often asymptomatic until the most advanced stages, when symptoms of uremia develop.
End-stage renal disease (ESRD) is irreversible loss of renal function requiring dialysis or transplantation typically due to severe progressive scarring in the kidney from any cause.
Nephrolithiasis refers to formation of stones in the colecting system and is manifested by renal colic and hematuria (without red cell casts).
Urinary tract infection (UTI) is characterized by bacteriuria and pyuria (bacteria and leukocytes in the urine). It may be symptomatic or asymptomatic, and may affect the kidney (pyelonephritis) or the bladder (cystitis) only.
visceral epithelium capillary wallwhereas the parietal epithelium encircles Bowman space (urinary space), the cavity in which filtrate of plasma collect
units of glomerular capillary
Fenestrated endothelial cells, with each fenestra being 70 to 100 nm in diameter.
• The glomerular basement membrane (GBM), which has a thick, electron-dense central layer (lamina densa), and two thinner, electron-lucent peripheral layers, the lamina rara interna and lamina rara externa. The GBM consists of collagen (mostly type IV), laminin, polyanionic proteoglycans, fibronectin, & gp’s.
• Podocytes, cells that possess interdigitating foot processes that are embedded in and adherent to the lamina rara externa. Adjacent foot processes are separated by 20- to 30-nm–wide filtration slits, which are bridged by a thin slit diaphragm composed mainly of the protein nephri.
• Mesangial cells, which lie in a mesangial matrix between the capillaries that supports the glomerular tuft. These cells, of mesenchymal origin, are contractile and are capable of proliferation, of laying down collagen and other matrix components, and of secreting a number of biologically active mediators in response to cytokines.
