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Flashcards in Renal Pathology part 1 Deck (64)
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Most glomerular diseases are

immunologically mediated


Tubular and interstitial disorders are

frequently caused by toxic or infectious agents


Severe glomerular damage impaires

flow through the peritubular vascular system


Tubular destruction

-may induce glomerular injury by increasing intraglomerular pressure



-biochemical abnormality that refers to an elevation of BUN and creatinine levels and is related largely to a decreased glomerular filtration rate (GFR)
-consequence of renal and external disorders
-typical feature of both acute and chronic injury


Prerenal azotemia

Encountered where there is hypoperfusion of the kidneys (hypertension or excessive fluid losses from any cause, or if the effective intravascular volume is decreased due to shock, volume depletion, congestive heart failure or cirrhosis of the liver) that impairs renal function in the absence of parenchymal damage


Postrenal azotemia

-seen whenever renal flow is obstructed distal to kidney
-relief of obstruction followed by correction of the azotemia



-when azotemia becomes associated with clinical signs/symptoms and biochemical abnormalities
-failure of excretory function and a host of metabolic and endocrine alterations resulting from renal damage


Uremic patients frequently have secondary involvement of

-GI system (uremic gastroenteritis)
-peripheral nerves (peripheral neuropathy)
-heart (uremic fibrinous pericarditis)


Nephritic syndrome

-clinical entity caused by glomerular disease and is dominated by the acute onset of either grossly visible hematuria (RBCs in urine) or microscopic hematuria with dysmorphic red cells and red cell casts on urinalysis, diminished GFR, mild to moderate proteinuria, and hypertension
-classic presentation of acute post streptococcal glomerulonephritis


Rapidly progressive glomerulonephritis

-nephritic syndrome with rapid decline in GFR (within hours to days)


Nephrotic syndrome

-due to glomerular disease
-heavy proteinuria, hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria


Asymptomatic hematuria/proteinuria

usually a manifestation of subtle or mild glomerular abnormalities


Acute kidney injury

-Rapid decline in GFR (within hours to days), with concurrent dysregulation of fluid and electrolyte balance, and retntion of metabolic waste products normally excreted by the kidney including urea and creatinine
-In most severe forms, manifested by oliguria or anuria (reduced or no urine flow)


Acute kidney injury can result from

-glomerular, interstitial, vascular or acute tubular injury


Chronic kidney disease

-the presence of a diminished GFR that is persistently less than 60mL/min/ 1.73 m2 for at least 3 months, from any cause, and/or persistent albuminuria
-may present with clinically silent decline in renal excretory function in milder forms and in more severe cases by prolonged symptoms and signs of uremia
-end result of all chronic renal parenchymal diseases


end stage renal disease (ESRD)

-GFR less than 5% of normal; terminal state of uremia


Renal tubular defects are dominated by

polyuria (excessive urine formation), nocturia, and electrolyte disorders (metbolic acidosis)
-result of diseases that with either directly affect tubular structures or cause defects in specific tubular functions (can be inherited or acquired)


Urinary tract infection

-bacteriuria and pyuria
-may be symptomatic or asymptomatic, may affect the kidney or the bladder



-renal stones
-spasms of severe pain (renal colic) and hematuria,often with recurrent stone formation


Secondary glomerular disease causes

-systemic immunologic diseases such as systemic lupus erythmatous, vascular disorders such as hypertension, metabolic diseases such as diabetes mellitus, and some heriditary conditions such as Fabry disease often affect glomerulus


The glomerulus consists of

-an anastomosing network of capillaries lined by fenestrated endothelium invested by 2 layers of epithelial cells
-visceral epithelial cells (podocytes) are incorporated into and become an intrinsic part of the capillary wall, separated from endothelial cells by a basement membrane


Glomerulus parietal epithelium

-situated on Bowman's capusule
-lines the urinary space, the cavity in which plasma filtrate first collects


The glomerular capillary wall is

-the filtering membrane and consists of a thin layer of fenestrated endothelial cells, a glomerular basement membrane (GBM) with a thick electron-dense layer, the lamina densa, and thinner electron-lucent peripheral layers, the lamina rara internal and lamina rara external


GBM consists of

-collagen type IV, laminin, polyanionic proteoglycans (mostly heparin sulfate), fibronectin, entactin, and several other glycoproteins


Type IV collagen forms

-a network suprastructure to which other glycoproteins attach
-building block of this network is a triple-helical molecular composed of one or more of 6 types of alpha chains
-each molecule consists of a 7s domain at the N terminus, a triple-helical domain in the middle, and a globular non collagenous domain (NC1) at the C terminus


NC1 domain

-importain for helix formation and for assembly of collagen monomers into the basement membrane superstructure
-glycoproteins and proteoglycans attach to the collagenous superstructure


Antigens in the NC1 domain are

the targets of Abs in the anti-GBM nephritis; genetic defects in the alpha chains underly some forms of heriditary nephritis; and the proteoglycans content of the GBM may contribute to its permeability characteristics


Visceral epithelial cells (podocytes)

-possess interdigitating processes embedded in and adherent to the lamina rara externa of the basement membrane
-adjacent foot processes are separated by filtration slits, which are bridged by a thin diaphragm


Glomerular tuft is supported by

mesangial cells lying between the capillaries