Kidney nontumor

General

Renal disease-general



Topic Completed: 2 April 2012

Minor changes: 10 March 2021

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PubMed Search: Renal disease nontumor

Nikhil Sangle, M.D.
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Cite this page: Sangle N. Renal disease-general. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/kidneyrenaldisease.html. Accessed December 8th, 2021.
Renal disease
  • 20% of women get urinary tract infections
  • 1% of Americans develop renal stones
  • Divided for analytical purposes into diseases of glomeruli, tubules, interstitium and vessels
  • Glomerular diseases tend to be immunologically mediated; tubular and interstitial disorders are often due to toxins / infections
  • Glomerular and tubular disease affect each other because glomerular disease impairs the tubular blood supply and increases tubular toxins and tubular disease causes increased intraglomerular pressure
  • Acute nephritic syndrome:
    • Grossly visible hematuria, hypertension, azotemia, oliguria, mild edema, red blood cell casts and variable proteinuria (Wikipedia: Nephritic syndrome)
    • Associated with postinfectious glomerulonephritis, early lupus, diffuse crescentic and membranoproliferative glomerulonephritis
  • Acute renal failure:
    • Abrupt anuria or oliguria with rapidly progressive azotemia identified by increase in BUN (blood urea nitrogen) or ammonia
  • Azotemia:
    • Increased serum BUN and creatinine due to reduced GFR (glomerular filtration rate)
    • Causes are prerenal (hemorrhage, shock, congestive heart failure, volume depletion), renal and postrenal (obstruction)
  • Chronic renal failure:
    • Azotemia progressing to uremia over a period of years
    • Stages of chronic renal failure:
      • Diminished renal reserve (GFR 50% normal) with normal BUN/creatinine
      • Renal insufficiency: azotemia, anemia, hypertension, polyuria and nocturia
      • Renal failure: GFR < 20% normal, kidneys cannot regulate volume of solutes and patient develops edema, metabolic acidosis and hypocalcemia
      • End stage renal disease: GFR < 5% normal, represents the end stage of various renal diseases
  • Nephrotic syndrome:
    • Proteinuria > 3.5 g/day, hypoalbuminemia (serum level < 3 g/dl), hyperlipidemia, lipiduria and severe edema (anasarca)
    • Due to derangement in glomerular capillary walls, which leads to increased permeability to plasma proteins, causing massive (nonselective) proteinuria, microhematuria in 50%, hypoalbuminemia and generalized edema (pitting, periorbital and dependent edema), hypertension in up to 25% and thrombotic tendency
    • Hyperlipidemia is due to increased lipoprotein synthesis and decreased catabolism
    • Lipiduria is due to leakage of lipoproteins with albumin
    • Patients are prone to staphylococcus and pneumococcal infections due to loss of immunoglobulins and factor B of complement
    • Thrombosis and thromboemboli are due to loss of anticoagulants such as antithrombin III and antiplasmin
    • Associated with minimal change disease (more common in children), focal and segmental glomerulosclerosis, membranous glomerulonephritis (more common in adults), systemic disease (SLE, diabetes, amyloidosis) and congenital nephrotic syndrome
  • Uremia:
    • Azotemia plus clinical signs / symptoms (gastroenteritis, peripheral neuropathy, fibrinous pericarditis, secondary hyperparathyroidism); associated with chronic renal failure
    • Tubular defects cause polyuria, nocturia and electrolyte disorders; due to diseases directly or indirectly affecting tubular function
Glomerular disease
  • Glomerulonephritis: inflammation of glomerulus
  • Glomerulopathy: any disorder affecting glomerulus
  • Primary: kidney is only or predominant organ involved
  • Changes can be diffuse (all glomeruli) or focal; global (entire glomerulus) or segmental (part of glomerulus) or mesangial
  • Minimal change disease, diffuse mesangial hypercellularity and focal and segmental glomerulosclerosis may be a continuum of the same disease
  • EGFR pathway may be new therapeutic target in glomerular disease (Nephrol Dial Transplant 2012;27:1297)
  • Pathogenesis of glomerular disease:
    • Usually immune mediated via antibody deposition, cell mediated injury or activation of alternative complement pathway (Nephrol Dial Transplant 1998;13:10, Medchrome: Pathogenesis of Glomerular Injury [Accessed 12 February 2020])
    • Antibodies deposited are either to in situ antigen (intrinsic or planted) or are circulating immune complexes
    • Intrinsic: Goodpasture disease antigens are in basement membrane; Heymann nephritis antigens are on visceral epithelial cells; produce linear immunofluorescence patterns
    • Planted antigens are deposited in basement membrane; may be exogenous (drugs, infectious agents) or endogenous (DNA, immunoglobulin, immune complexes); their cationic proteins bind to glomerular anionic sites and produce granular lumpy staining by immunofluorescence
    • Circulating immune complexes may be endogenous (DNA, tumors) or exogenous (infectious products); they usually localize within glomeruli and activate complement; deposits are usually mesangial or subendothelial and resolve by macrophage phagocytosis, unless there are repeated cycles of formation (Hepatitis B / C, lupus)
    • Cell mediated immune injury is by sensitized nephritogenic T cells
    • Progression to end stage renal disease occurs when the glomerular filtration rate (GFR) is 30 - 50% of normal, due to compensatory hypertrophy of remaining glomeruli and systemic hypertension (inhibited by angiotensin converting enzyme inhibitors), eventually causing glomerulosclerosis
  • Micro description: injured epithelial cells have vacuoles, retract and detach from basement membrane, lose foot processes
  • Immunofluorescence description: granular deposits represent immune complexes that settle out of blood or form in situ; linear deposits are due to antibasement membrane antibodies or light chain nephropathy; can detect via fluorescent antibodies or using fluorescence microscopy of H&E stained sections fixed in Hollande fixative (Mod Pathol 2002;15:988)
Chronic glomerulonephritis
  • An end stage disease, due to progression of various types of glomerulonephritis; occasionally no prior history of kidney disease (eMedicine: Chronic Glomerulonephritis [Accessed 12 February 2020])
  • Rates of progression: rapidly progressive (90%), post streptococcal (1% children, 5% adults), focal and segmental glomerulosclerosis (50 - 80%, rapid), membranous (50%), membranoproliferative (50%), IgA nephropathy (30 - 50%, slow)
  • Paradoxically, nephrotic syndrome symptoms decrease as glomeruli disappear
  • Gross description: symmetrically small kidneys with thin granular cortex and increased peripelvic fat
  • Micro description: glomerulosclerosis, tubular atrophy and thyroidization, interstitial fibrosis and lymphocytic inflammation; arterial and arteriolar sclerosis
Tubular and interstitial disease
  • Primary tubulointerstitial disease (nephritis) lacks significant glomerular or vascular injury; causes 20 - 40% of cases of end stage renal disease (eMedicine: Tubulointerstitial Nephritis [Accessed 03 January 2018])
  • Secondary tubulointerstitial nephritis is due to glomerular disease, systemic or vascular disorders
  • Tubulointerstitial disease may be acute (interstitial edema, neutrophils, focal tubular necrosis) or chronic (mononuclear inflammation, interstitial fibrosis, tubular atrophy)
  • Symptoms: inability to concentrate urine (polyuria, nocturia), salt wasting and diminished ability to excrete acids (metabolic acidosis)
  • Causes: infections, jejunoileal bypass (Arch Pathol Lab Med 1980;104:112) metabolic disease, toxins, tumors, vascular diseases
  • IgG4 staining recommended to identify subset with IgG4 related disease (Clin Nephrol 2011;76:440)
Case reports
Microscopic (histologic) description
  • Hypercellularity: due to cellular proliferation (mesangial, endothelial, parietal epithelial cells); white blood cells (acute and chronic) or crescents (white blood cells and epithelial cells)
  • Basement membrane thickening is highlighted by PAS stain and electron microscopy; EM also shows electron dense deposits (usually immune complexes) in or adjacent to basement membrane (subepithelial is most common)
  • Hyalinization and sclerosis of glomeruli are the end result of glomerular damage from various causes
Microscopic (histologic) images

Acute interstitial nephritis
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Interstitial inflammation

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Interstitial inflammation with eosinophils

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Chronic glomerulonephritis

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