Important terminology Flashcards
Azotemia
a biochemical abnormality referring to an elevation of blood urea nitrogen (BUN) and creatinine levels usually secondary to a decreased glomerular filtration rate (GFR).
Prerenal azotemia when there is hypoperfusion of the kidneys
Postrenal azotemia is associated with urine flow obstruction
Uremia
is azotemia plus numerous clinical findings in biochemical abnormalities resulting from renal damage
Nephritic syndrome
is caused by glomerular disease, associated with acute onset of hematuria, red cell casts, decreased GFR with azotemia and mild to moderate proteinuria and hypertension
Nephrotic syndrome
is caused by glomerular disease and is characterized by heavy proteinuria (>3.5 gm/day), hypoalbuminemia, severe edema, hyperlipidemia and lipiduria.
Asymptomatic hematuria or proteinuria
is usually a manifestation of mild glomerular abnormalities.
Normal urine output
1-2.5 L per day
Polyuria
urine output greater than 2.5 L per day (diabetes, increase water ingestion)
Oliguria
urine output less than 400 mL per day (acute glomerulonephritis, renal failure)
Anuria
urine output less than 100 mL per day (renal shutdown)
Acute kidney injury
is characterized by a rapid decline in GFR (within hours to days), concurrent dysregulation of fluid and electrolytes and retention of metabolic waste products (urea and creatinine). In most severe forms is manifested by oliguria or anuria (reduced or no urine flow). It can result from glomerular, interstitial, vascular or acute tubular injury. (Increase in serum creatinine)
Chronic kidney disease
is defined as the presence of decreased GFR that is persistently less than 60 ml/min/1.73 m2 for at least three months from any cause and/or persistent albuminuria.
Chronic glomerulonephritis
refers to end-stage glomerular disease that may result from specific types of glomerulonephritis or may develop without antecedent history of any of the well-recognized forms of acute glomer¬ulonephritis.
End-stage renal disease
(ESRD) GFR is less than 5% of normal
Renal tubular defects
are dominated by polyuria (excessive urine formation) and electrolyte disorder (metabolic acidosis) and are the result of diseases that directly affect tubular structure or functions.
Nephrolithiasis
(renal stones) is manifested by severe pain and hematuria and often associated with recurrent stone formation.
Mesangial cells
embedded in the mesangial matrix support the glomerular capillary tuft and are contractile, phagocytic and capable of proliferation and laying down both matrix and collagen. Can release inflammatory mediators and proliferate in disease
Parietal epithelial cells
make up the lining cells of Bowman’s capsule and the proliferation of parietal epithelial cells creates crescents in rapidly progressive glomerulonephritis.
Visceral epithelial cells (podocytes)
are important for the maintenance of glomerular filtration function and the slit diaphragm which presents a size selective distal diffusion barrier to the filtration of proteins and are largely responsible for the synthesis of glomerular basement membrane components.
Glomerular basement membrane
lies between the visceral epithelial cells and capillary lumen endothelial cells of the glomerular capillary tuft and consists of collagen (mostly type IV), laminin, proteoglycans and glycoproteins. Biochemical properties of the glomerular basement membrane are critical for understanding glomerular diseases.
Benign nephrosclerosis
describes renal pathology associated with sclerosis of renal arterioles and small arteries and is associated with slight decreased GFR and mild proteinuria
Malignant nephrosclerosis
is a renal vascular disorder associated with accelerated hypertension (systolic >200 mm Hg) and associated with papilledema, retinal hemorrhages, encephalopathy and cardiovascular abnormalities leading to renal failure
Mild glomerulonephritis
Mild glomerulonephritis is defined as a nephritic sediment in patients who have a normal or near normal estimated glomerular filtration rate and do not have the nephrotic syndrome.
Moderate to severe glomerulonephritis
defined as a nephritic sediment in patients who have a reduced estimated glomerular filtration rate and/or nephrotic syndrome.
Glomerular Hyperfiltration
occurs in a variety of different clinical conditions including kidney disease. No single definition has been agreed upon. Glomerular hyperfiltration because afferent arteriole vasodilation (diabetes) and efferent arteriole vasoconstriction (rennin angiotensin aldosterone system activation) leading to glomerular hypertension. Pregnancy, high protein meal, polycystic kidney disease, secondary focal segmental glomerulosclerosis, sickle cell anemia all can lead to glomerular hyperfiltration.