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.
Hereditary nephritis
refers to a group of heterogeneous familial renal diseases associated with mutations in collagen genes that manifest primarily with glomerular injury. Two deserve discussion: Alport syndrome, because the lesions and genetic defects have been well studied, and thin basement membrane lesion, the most common cause of benign familial hematuria.
Focal-
Involving
Diffuse
Involving ≥50% of glomeruli
Segmental-
Involving part of a glomerular tuft
Global-
Involving all of a glomerular tuft
Proliferative glomerulonephritis
has greater than 100 nuclei in affected glomeruli
Membranous glomerulonephritis
has thick glomerular basement membranes without proliferating cells
Membranoproliferative
Combined capillary wall thickening and mesangial or endocapillary hypercellularity
Focal segmental glomerular sclerosis
involves only a segment of the involved glomerulus
Primary glomerular disease
involves only glomeruli and no other target organs
Secondary glomerular disease
involves glomeruli and other target organs such as systemic lupus or diabetic mellitus
Mesangial hypercellularity
More than four nuclei in the contiguous matrix of a peripheral mesangial segment
Endocapillary hypercellularity
Increased cellularity internal to the GBM composed of leukocytes, endothelial cells, and/or mesangial cells
Extracapillary hypercellularity
Increased cellularity in Bowman’s space or more than one layer of parietal or visceral epithelial cells
Crescent extracapillary hypercellularity
other than the epithelial hyperplasia of collapsing variant of focal segmental glomerulosclerosis
Fibrinoid necrosis
Lytic destruction of cells and matrix with deposition of acidophilic fibrin-rich material
Sclerosis
Increased collagenous extracellular matrix that is expanding the mesangium, obliterating capillary lumens, or forming adhesions to Bowman’s capsule
Hyalin-
Glassy acidophilic extracellular material
Acute tubular necrosis
(often coagulative necrosis) usually secondary to toxins and/or ischemia. Also a clinicopathologic term used in ischemic nephropathy with only mild or subtle epithelial cell changes
Tubular casts
are various coagulated proteins and formed cellular elements in the tubular lumens (red blood cell, white blood cell, hyaline or pigmented casts)
Papillary necrosis
is usually bilateral and affects the tips or distal two thirds of the pyramids. Microscopic examination shows ischemic quagga necrosis. Papillary necrosis is seen mainly in diabetics, sickle cell disease and in those with urinary tract obstruction.
Pyonephosis
is seen with total urinary tract obstruction. There is a suppurative exudate that fills the renal pelvis, calyces and ureter with pus.
Perinephric abscess
is an extension of suppurative inflammation through the renal capsule into the perinephric soft tissues
Urinary tract infection
is an inflammatory response of the urothelium to bacterial tissue invasion and is usually associated with bacteriuria and pyuria
Bacteriuria
is the presence of bacteria in the urine which is normally free of bacteria
Pyuria
is the presence of white blood cells in the urine and is generally indicative of infection and or inflammatory response of the urothelium
Acute pyelonephritis
is a clinical syndrome of chills, fever and flank pain accompanied by bacteriuria and pyuria (generally indicative of bacterial infection of the kidney)
Chronic pyelonephritis
describes a shrunken scarred kidney secondary to primary renal disease or postinfectious
Selective proteinuria
is the increased excretion of medium-size negatively charged proteins such as albumin (usually indicates moderate glomerular damage)
Nonselective proteinuria
is the increased excretion of proteins of any size (usually indicates severe glomerular damage)
Hyaline casts
(Tamm-Horsfall proteins secreted from the tubular epithelial cells), most common casts that are formed normally (low urine flow, concentrated urine or acidic environment)
Granular casts
are the second most common casts. Well most often indicative of chronic renal disease, these casts can also be seen for a short time following strenuous exercise. Can be seen in acute tubular necrosis.
Waxy casts
are thought to represent and product of cast evolution and degeneration and suggest very low urine flow associated with severe long-standing kidney disease.
Pigmented granular casts
are formed by the adhesion of metabolic breakdown products or drug pigments giving the cast discoloration. Seen in rhabdomyolysis with myoglobinuria or rarely with hemoglobinuria
Red blood cell casts
are always pathological and strongly indicative of glomerulonephritis. Can be seen in vasculitis induced glomerulonephritis
White blood cell casts
are seen commonly in pyelonephritis and interstitial nephritis
Tubular cell casts
are seen with any acute tubular injury and other dominant cellular casts in ischemic acute tubular necrosis
