Medical kidney diseases

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This article describes medical renal disease or the medical kidney. Much in medical kidney depends on the clinical information. Most of the disease seen by pathologists is... glomerular disease. If in doubt... the answer to most questions is diabetes mellitus or systemic lupus erythematosus. Medical kidney is niche area in pathology. It is one of the few areas that routinely requires electron microscopy.

Kidney tumours are dealt with in the kidney tumours article.

Clinical

Glomerular filtration rate

  • Abbreviated GFR.
  • Ultimate measure of renal function.
  • Declines with age.
  • Normal range (dependent on age): 116-75 mL/min/1.73m2.[1]

Creatinine

  • The standard screening test for renal function.
  • 300 mmol/L is the general cut-point for referral to a nephrologist.[2]

Notes:

  • Dinosaurs use the units mg/dL; normal with these units is: 0.8 to 1.4 mg/dL.[3]
  • Conversion: 1.0 mg/dL = 88.4 umol/L.[4][5]

Urine protein to creatinine ratio

  • Indicator of proteinuria.
  • Predictor of glomerular filtration rate.[6]

Cut points:[7]

  • Normal (2 years and older): <0.2 g protein / g Creatinine
  • Nephrotic range: >3.5 g protein / g Creatinine.

Complement

C3, C4 levels:[8]

  • Changed:
    • Systemic lupus erythematosus (SLE); levels decreased = increased disease activity.
    • Post-infectious GN - decreased.
    • MPGN - decreased. (???)
    • Infection.[9][10]
    • Hemolytic anemia.[9][11]
  • Normal:
    • Minimal change disease.
    • Chronic pyelonephritis.
    • Renal vein thrombosis.
    • Amyloidosis.

Anti-MPO antibodies

  • MPO-ANCA associated with crescentic glomerulonephritis.[12]

C4d

  • Suggests humoral immunity (antibody-mediated immunity) at play.
  • Important in monitoring of renal transplant recipients.

Urine dip

Findings:[13]

  • RBC casts = acute bleed, e.g. nephritic syndrome.
  • WBC casts = interstitial nephritis, e.g. pylonephritis, parenchymal infection.
  • Hemegranular casts = acute tubular necrosis, transplant rejection.

Notes:

  • "Active sediment" = RBCs, RBC casts;[14] implies glomerulonephritis.
    • Some include the above (RBCs, RBC casts) + WBCs & protein.[15]

Urine crystals

Main article: Crystals in body fluids

Clinical presentations

Nephrotic syndrome

Features:

  • Anasarca (whole body - edema).
  • Proteinuria (>3.5 g/24h).
  • Hypercholesterolemia.
  • Hypoalbuminemia.

Nephritic syndrome

Features - mnemonic PHAROH:[16]

  • Proteinuria.
  • Hypertension.
  • Azotemia.
  • RBC casts.
  • Oliguria.
  • Hematuria.

Mixed

  • Features of nephritic syndrome and nephrotic syndrome.

Normal

Epithelium

Features:[17]

  • The glomeruli visceral epithelium is part of the capillary wall (part of the glomerular tuft).
  • The parietal epithelium is part of Bowman's capsule.

Remember: visceral has vessels.

Basic approach to renal biopsy

Basic components

  • Glomeruli.
  • Tubules.
  • Interstitium.
  • Vessels.

Glomeruli

  1. Mesangium
    • Matrix should be: "one cell thick" (expanded in diabetes mellitus).
    • Cellularity of the mesangium - normal = upto 3 cells (don't count cell abutting the capillary lumen, don't count at the hilum).
  2. Capillary loops "open"
    • Lumina patent? If not patent is it due to matrix or cells (endocapillary hypercellularity).
    • Capillary wall morphology - wavy thin is normal; hulla-hoop/wire-like abnormal (suggestive of immune complex deposition).
  3. Bowman's space (urinary space) - crescents present?
  • Count the number of glomeruli.
  • Count number of the obsolete glomeruli.

Components of the glomeruli (anatomical)

  • Podocyte - rarely affect by disease
    • One notable disease is collapsing glomerulopathy in HIV.[18]
  • Endothelial cell.
  • Mesangial cell.

Vessels

  1. Arteriolar hyalinosis - too much pink stuff?
  2. Intimal hyperplasia.

Consider:

  • Vasculitis? - inflammatory cells in vessel wall.
  • Amyloid? - pink.
  • Rejection? - PMNs.

Tubules & interstitium

Tubules - proximal portion is the most important.

  • Casts?
  • Necrosis?

Interstitium

  • Fibrosis - prognostically important.
    • Grading: mild = <25%, moderate 25-50%, severe >50%.

Important terms/process related

Obsolete glomeruli

  • Completely sclerosed glomeruli are not important - unless present in larger numbers than expected for the age of the patient.
Percent of sclerosed glomeruli = (age in years)/2 - 10%.[19]

Example:

  • It is normal for an 80 year-old to have 30% sclerosed glomeruli.

Glomerular disease terms[20]

  • Global = >50% of glomeruli.
  • Focal = <50% of glomeruli.
  • Segmental = part of glomerulus.
  • Diffuse = most of glomerulus.

Staining

The standard stain in kidney pathology is PAS. Section are usually 1-2 micrometers, as opposed to 4-5 micrometers seen in rountine section of other organs.

Interpretation of medical renal disease more difficult or even impossible if the sections are thicker, as one does not see the glomerular structures well.

In kidney that is cut thick the glomeruli look more nodular and it is more difficult to find open capillary loops.

Immunofluorescence

Routinue (mnemonic GAM CF):

  • IgG.
  • IgA.
  • IgM.
  • C3.
  • Fibrinogen.

Optional:

  • Kappa.
  • Lambda.

Immune complex-related disease

Can be:

  • Subepithelial - distal to basement membrane (BM), closer to the urinary space.
  • Subendothelial - proximal to BM, closer to the glomerular capillary.

Tram-tracking of BM

DDx:[21]

  1. MPGN.
  2. Thrombotic microscopic angiopathy (TMA).
  3. Transplant glomerulopathy (TG).

Arteriolar hyalinosis

Microscopic:

  • Pink acellular crap replaces arteriolar wall.

DDx:

  • Diabetes mellitus.
  • Hypertension.
  • Aging.
  • Drugs - tarolimus, cyclosporine.

Note:

  • Arteriolar hyalinosis - involves afferent and efferent arterioles in diabetes, in others it is only tha afferent.

Mesangial hypercellularity

DDx:

  1. Lupus (SLE).
  2. IgA nephropathy.

Mesangial expansion

  • Diabetes mellitus.[22]
  • Immune complex mediated disease (e.g. IgA nephropathy).
  • Henoch-Schoenlein disease.
  • Lupus.

Bland necrotic crescents

DDx:

  • ANCA-related glomerulonephritis.
  • Anti-GBM disease.

Diseases with crescents - is a long list.[23]

Pathologic DDx

The clinical presentations suggest a pathologic DDx.[24]

Nephritic

  • Post-infectious glomerulonephritis.
    • Classically streptococcal.
  • Crescentic glomerulonephritis (AKA rapidly progressive glomerulonephritis (RPGN)).
    • Anti-GBM disease.
    • ANCA disease (e.g. Wegener's granulomatosis).
    • Goodpasture's syndrome.

Nephrotic

  • Minimal segmental disease (MSD) - AKA minimal change disease (MCD).
  • Focal segmental glomerulosclerosis (FSGS).
  • Membranous nephropathy.

Mixed presentation

  • IgA nephropathy,
  • Focal proliferative glomerulosclerosis (FPGS).
  • Membranoproliferative glomerulonephritis (MPGN).


Patterns - Table

Pattern Key feature Other findings IF & EM Presentation Clinical Pathol. DDx Image
Nodular GS nodular mesangial matrix expansion GBM thickening, both afferent and efferent arteriole hyalinzed EM? presentation? diabetes mellitus membranous nephropathy (?) Image?
Focal segmental GS (FSGS) focal sclerosis of glom +/-interstitial fibrosis EM? nephrotic syndrome primary FSGS, secondary FSGS; unresponsive to steroids, worse prognosis than MCD Pathol. DDx? Image?
Membranous nephropathy
(AKA membranous GN) 		Gloms with wire loops mesangial hypercellularity EM? nephrotic syndrome hep B, hep C, carcinoma, NSAID toxicity, SLE, idiopathic Nodular GS (?) Image?
Minimal change disease (MCD) EM changes usu. none EM changes nephrotic syndrome idiopathic vs. secondary; idiopathic responds to steroids Pathol. DDx? Image?
IgA nephropathy +ve IF for IgA +/-mesangial hypercellularity (???) IgA +ve mixed nephrotic/nephritic Clinical? Pathol. DDx? Image?
Membranoproliferative GN (MPGN) thick GBM Other findings? subepithelial deposits mixed nephrotic/nephritic Clinical? Pathol. DDx? Image?
Focal proliferative
glomerosclerosis (FPFS) 		<50% of glomeruli partially sclerosis Other findings? EM? mixed nephrotic/nephritic Clinical? Pathol. DDx? Image?
Rapidly progressive GN (RPGN) cresents Other findings? EM? nephritic syndrome Clinical? Pathol. DDx? Image?

Nephrotic syndrome

A broad classification of nephrotic syndrome based on etiology:

 
 
 
Nephrotic
syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Primary
 
 
 
Secondary

In children nephrotic syndrome is assumed to be minimal change disease. Biopsies are done only there is no response to steriods.

Diseases

Diabetes mellitus

General

  • Most common cause of end stage renal disease (ESRD).
  • Rarely biopsied.

Microscopic

Features:[25]

  • Thick glomerular basement membrane (GBM).
  • Thickened (eosinophilic) tunica media in both the afferent and efferent arterioles.[26]
  • Mesangial matrix expansion - leads to nodule formation Kimmelstiel-Wilson nodules (nodular glomerulosclerosis).

Other:

  • Armanni-Ebstein change - cytoplasmic vacuolization of tubular cells (usu. loop of Henle) -- innermost cortex, outer medulla;[27] not specific to diabetes mellitus.[28]

Other - with weak evidence:

  • Extra efferent vessels.[29]

Memory device:

  • GBM = thick GBM, both afferent & efferent artiole thickened, mesangial matrix expansion.

Images:

Notes:

  • Hypertensive kidneys have changes only in the afferent arteriole, i.e. the efferent arteriole is spared (see hypertension).

Lupus nephritis

General

  • Abbreviated LN.
  • Bread & butter of nephropathology.

Immunofluorescence

  • "Full house" = call of 'em light up.

Classification

International Society of Nephrology/Renal Pathology Society (ISN/RPS) classification:[30][31]

  • Class I - minimal mesangial LN.
  • Class II - mesangial proliferative LN.
  • Class III - focal lupus nephritis; <50% of glomeruli.
  • Class VI - diffuse segmental or global LN; >50% of glomeruli.
  • Class V - Membranous lupus nephritis.
  • Class IV - Advanced sclerosing LN; essentially end-stage kidney.

Notes:

  • Most of the action is in Class III and Class IV.
    • Class I is near normal - doesn't get biopsied.
    • Class IV is essentially dead kidney - doesn't get biopsied.

Nephrotic syndrome

Focal segmental glomerulosclerosis

General

  • Abbreviated FSGS.
  • Presents as nephrotic syndrome.
  • Does not respond to steroids (unlike MCD).

Etiology

  • Primary.
    • May be familial.[32]
  • Secondary.[33]
    • HIV.
    • Drug use.
    • Reduced renal mass.

Primary vs. secondary:[34]

Feature Primary Secondary
Proteinuria (onset) sudden progressive
Albumnin low normal
Glomerulus size normal increased
Foot process effacement diffuse mild

Microscopic

Features:

  • Partial sclerosis of less than 50% of glomeruli.

Image:

Histologic classification

FSGS can be subdivided into the following subgroups:[35]

  • Cellular.
  • Collapsing - poor prognosis.
  • Tip lesion - good prognosis.
  • Perihilar.
  • Not otherwise specified (NOS) - most common.

Stains

Features:[36]

  • PAS +ve crescents.

Membranous nephropathy

General

  • AKA membranous glomerulonephritis.
  • Presents as nephrotic syndrome.

Clinical DDx:[37]

  • Hepatitis B.
  • Hepatitis C.
  • Carcinoma.
  • NSAID toxicity.
  • SLE.
  • Idiopathic.

Microscopic

Features:

  • Subepithelial immune complex depositions, spike forming.

Image:

Mixed nephrotic and nephritic=

IgA nephropathy

General

  • AKA Berger disease.
  • More common in Asians.

Microscopic

Features:

  • Mesangial hypercellularity - may be only light microscopy finding.
  • Diagnosis based on immunofluorescence (IgA+).

Image: IgA nephropathy (med.utah.edu).

Scoring

IgA nephropathy can be scored using an assessment of mesangial proliferation, endocapillary proliferation, glomerulosclerosis and tubular atrophy and interstitial fibrosis (abbreviated MEST).[38]

Membranoproliferative glomerulonephritis

General

  • Abbreviated MPGN.
  • In adults most common cause: hepatitis C.

Microscopic

Features:

  • Endothelial cell proliferation.
  • Basement membrane double layering (tram-tracking).
  • Mesangial hypercellularity.

Nephritic syndrome

Rapidly progressive glomerulonephritis

  • Abbreviated RPGN.

General

  • Acute renal dysfunction.

DDx:

  • Post-infectious GN.
  • Pauci-immune GN.

Microscopic

Features:

  • Crescents.
  • +/-Neutrophils (suggestive of post-infectious GN).

Image:

Rare diseases

Fabry disease

General

  • Rare X-linked genetic disease.
    • Caused by defect in alpha-galactosidase A gene.
    • Women partially affected
  • Lysosomal storage disorder -- 2nd in prevalence only to Gaucher disease.
  • Multisystem disease affecting small vessels and kidney.

Presentation

  • Women: usually proteinuria.
  • Men: angiokeratomas (skin lesion), proteinuria.

Tx

  • Symptomatic treatment.
  • Enzyme replacement - agalsidase alpha (Replagal) or agalsidase beta (Fabrazyme).

Microscopy

LM:[39]

  • Foamy podocyte inclusions, best visualized with toluidine blue.
  • Mild mesangial hypercellularity.

EM:[39]

  • Myelin-like inclusions.
    • Concentric bodies with an onion-skin-like appearance.
  • Zebra bodies.
    • Ovoid inclusions with striped pattern.

Note:

  • Myelin-like inclusion are not pathognomonic for Fabry disease; they may result from drug use:[39]
    • Amiodarone,
    • Aminoglycosides,
    • Chloroquine.

Pyelonephritis

General

  • Usually diagnosed clinically: urine C&S, urine R&M, +/-CT abdomen.

Gross

Features:[40]

Microscopic

Features:

  • Interstitial nephritis.

Acute tubular necrosis

General

  • Best diagnosed clinically (using urine R&M) - hemegranular casts are diagnostic.
  • Often abbreviated ATN.

Microscopic

Features:[41]

  • Hemegranular casts in the lumen.
  • Regenerative activity (mitoses).

Hepatorenal syndrome

  • Acute renal failure due secondary to cirrhosis or fulminant liver failure.

Clinical

  • Urine sodium is low,[42] unlike in ATN (the main DDx).

Pathophysiology

  • Renal vasoconstriction.[43]

Histology

  • Normal.

Treatment

Medical and surgical:[44]

  • Vasoconstrictors (e.g. midodrine, terlipressin (counteracts splanchnic vasodilation), norepinephrine).
  • Albumin.
  • TIPS (transjugular intrahepatic portosystemic shunt).
  • Liver transplantation.

Note:

  • I suspect a portal vein pump would work... it reduces portal pressure and would likely increase hepatic function.

Alport disease

Clinical

  • Hearing loss (sensorineural).
  • Hematuria - usually preceeds hearing loss.[45]
  • Can be thought of a pathologic form of thin basement membrane disease.[46]

Etiology

  • Genetic defect - collagen type IV.

Inheritance:[45]

  • X-linked - 80%.
  • Autosomal recessive - 15%.
  • Autosomal dominant - 5%.

Myeloma

See: haematopathology.

Cast nephropathy

Features:

  • Cast with cellular reaction.
    • Macrophages (CD68 +ve).

Stains:

  • Myeloma casts = PAS -ve.
    • Hyaline casts = PAS +ve.

Microscopic

Features:[47]

  • Crap in tubules.
    • Refractile.

Image:

Amyloidosis

  • Usually associated with lambda clone.

Light chain deposition

  • Usually associated with kappa clone.

Cystic kidney diseases

Main article: Cystic kidney diseases

These are discussed in a separate article and include:

  • Autosomal dominant polycystic kidney disease (ADPKD).
  • Adult-onset medullary cystic disease.
  • Acquired renal cystic disease.
  • Autosomal recessive polycystic kidney disease (ARPKD).
  • Medullary sponge kidney.
  • Nephronophthisis.
  • Cystic renal cell carcinoma.

Transplant

General

Rejection can be:

  • Acute.
  • Chronic.
  • Acute-on-chronic.

Acute

  • Acute rejection has a standardized classification Banff classification.[48]

Diagnosis of acute rejection requires:

  1. Serology.
  2. IHC (C4d).
    • This is somewhat debated.
  3. Morphology.

Predictors

  • Associated with C4d+ IHC.[49]
  • Mean graft survival is ~4 years for C4d+ interstitial capillaries vs. ~8 years for C4d- renal grafts.[50]

Polyomavirus

  • This bad-boy is associated with failure of transplanted kidneys.[51]
  • Treatment: reduce immunosuppression.[52]

Microscopic features:[52]

  • Ground glass-like nuclear inclusions.
  • Nuclear enlargement.

Calcineurin-inhibitor toxicity

  • Calcineurin-inhibitors (e.g. cyclosporine,[53], tacrolimus[54]) toxicity can induce a thrombotic microangiopathy.
  • Hyaline arteriopathy with a peripheral and nodular distribution (chronic toxicity).

See also

References

  1. ↑ URL: http://www.kidney.org/professionals/KLS/gfr.cfm. Accessed on: 8 November 2010.
  2. ↑ Mendelssohn DC, Barrett BJ, Brownscombe LM, et al. (August 1999). "Elevated levels of serum creatinine: recommendations for management and referral". CMAJ 161 (4): 413–7. PMC 1230545. PMID 10478168. http://www.cmaj.ca/cgi/content/full/161/4/413.
  3. ↑ URL: http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm. Accessed on: 8 November 2010.
  4. ↑ URL: http://www.sydpath.stvincents.com.au/other/Conversions/ConversionMasterF3.htm. Accessed on: 8 November 2010.
  5. ↑ URL: http://www.unc.edu/~rowlett/units/scales/clinical_data.html. Accessed on: 8 November 2010.
  6. ↑ Ruggenenti P, Gaspari F, Perna A, Remuzzi G (February 1998). "Cross sectional longitudinal study of spot morning urine protein:creatinine ratio, 24 hour urine protein excretion rate, glomerular filtration rate, and end stage renal failure in chronic renal disease in patients without diabetes". BMJ 316 (7130): 504–9. PMC 2665663. PMID 9501711. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665663/pdf/9501711.pdf.
  7. ↑ URL: http://www.fpnotebook.com/urology/lab/urnprtntcrtnrt.htm. Accessed on: 8 November 2010.
  8. ↑ Levo Y, Pick AI (1974). "The significance of C3 and C4 complement levels in lupus nephritis". Int Urol Nephrol 6 (3-4): 233–8. PMID 4549215. http://www.springerlink.com/content/l1657797661468g1/fulltext.pdf.
  9. ↑ 9.0 9.1 Nusinow SR, Zuraw BL, Curd JG (May 1985). "The hereditary and acquired deficiencies of complement". Med. Clin. North Am. 69 (3): 487–504. PMID 3892188.
  10. ↑ URL: beckmancoulter.com. Accessed on: 9 November 2010.
  11. ↑ URL: beckmancoulter.com. Accessed on: 9 November 2010.
  12. ↑ Arahata, H.; Migita, K.; Izumoto, H.; Miyashita, T.; Munakata, H.; Nakamura, H.; Tominaga, M.; Origuchi, T. et al. (1999). "Successful treatment of rapidly progressive lupus nephritis associated with anti-MPO antibodies by intravenous immunoglobulins.". Clin Rheumatol 18 (1): 77-81. PMID 10088959.
  13. ↑ URL: http://www.nlm.nih.gov/medlineplus/ency/article/003586.htm. Accessed on: 20 September 2010.
  14. ↑ URL: http://emedicine.medscape.com/article/238158-overview. Accessed on: 9 November 2010.
  15. ↑ URL: http://www.nephrologychannel.com/agn/index.shtml. Accessed on: 9 November 2010.
  16. ↑ URL: http://books.google.com/books?id=5bmg8xiLxkMC&pg=PA249&lpg=PA249&dq=Nephritic+syndrome+PHAROH#v=onepage&q=Nephritic%20syndrome%20PHAROH&f=false. Accessed on: 9 December 2009.
  17. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 956. ISBN 0-7216-0187-1.
  18. ↑ AH. 13 August 2009.
  19. ↑ Fogo, Agnes B.; Kashgarian, Michael (2005). Diagnostic Atlas of Renal Pathology: A Companion to Brenner and Rector's The Kidney 7E (1st ed.). Saunders. pp. 16. ISBN 978-1416028710.
  20. ↑ Fogo, Agnes; Bruijn, Jan A.; Cohen, Arthur H.; Colvin, Robert B.;Jennette, J. Charles (2006). Fundamentals of Renal Pathology (1st ed.). Springer. pp. 82. ISBN 978-0387311265.
  21. ↑ AH. 17 July 2009.
  22. ↑ Fioretto P, Mauer M (March 2007). "Histopathology of diabetic nephropathy". Semin. Nephrol. 27 (2): 195-207. doi:10.1016/j.semnephrol.2007.01.012. PMID 17418688.
  23. ↑ URL: http://path.upmc.edu/cases/case51/dx.html. Accessed on: 9 November 2010.
  24. ↑ URL: http://www.emedicine.com/med/topic886.htm and http://www.emedicine.com/ped/topic1564.htm. Accessed on: 8 November 2010.
  25. ↑ Zelmanovitz T, Gerchman F, Balthazar AP, Thomazelli FC, Matos JD, Canani LH (2009). "Diabetic nephropathy". Diabetol Metab Syndr 1 (1): 10. doi:10.1186/1758-5996-1-10. PMC 2761852. PMID 19825147. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2761852/.
  26. ↑ Østerby R, Hartmann A, Bangstad HJ (April 2002). "Structural changes in renal arterioles in Type I diabetic patients". Diabetologia 45 (4): 542–9. doi:10.1007/s00125-002-0780-2. PMID 12032631.
  27. ↑ RITCHIE S, WAUGH D (1957). "The pathology of Armanni-Ebstein diabetic nephropathy". Am. J. Pathol. 33 (6): 1035–57. PMC 1934668. PMID 13478656. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934668/?page=1.
  28. ↑ Zhou C, Byard RW (September 2010). "Armanni-Ebstein phenomenon and hypothermia". Forensic Sci Int. doi:10.1016/j.forsciint.2010.08.018. PMID 20875709.
  29. ↑ Stout LC, Whorton EB (August 2007). "Pathogenesis of extra efferent vessel development in diabetic glomeruli". Hum. Pathol. 38 (8): 1167–77. doi:10.1016/j.humpath.2007.01.019. PMID 17490718.
  30. ↑ Weening JJ, D'Agati VD, Schwartz MM, et al. (February 2004). "The classification of glomerulonephritis in systemic lupus erythematosus revisited". J. Am. Soc. Nephrol. 15 (2): 241–50. PMID 14747370. http://www.nature.com/ki/journal/v55/n2/full/4490631a.html.
  31. ↑ URL: http://www.med.niigata-u.ac.jp/npa/Lectures/Lupus_Nephritis.htm. Accessed on: 9 November 2010.
  32. ↑ Sánchez de la Nieta MD, Arias LF, Alcázar R, et al. (2003). "[Familial focal and segmentary hyalinosis]" (in Spanish; Castilian). Nefrologia 23 (2): 172–6. PMID 12778884.
  33. ↑ URL: http://www.kidneypathology.com/English_version/Focal_segmental_GS.html. Accessed on: 11 February 2011.
  34. ↑ D'Agati, V. (Mar 2003). "Pathologic classification of focal segmental glomerulosclerosis.". Semin Nephrol 23 (2): 117-34. doi:10.1053/snep.2003.50012. PMID 12704572.
  35. ↑ Thomas, DB.; Franceschini, N.; Hogan, SL.; Ten Holder, S.; Jennette, CE.; Falk, RJ.; Jennette, JC. (Mar 2006). "Clinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic variants.". Kidney Int 69 (5): 920-6. doi:10.1038/sj.ki.5000160. PMID 16518352.
  36. ↑ URL: http://www.kidneypathology.com/English_version/Focal_segmental_GS.html. Accessed on: 11 February 2011.
  37. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 241. ISBN 978-1416002741.
  38. ↑ Coppo, R.; Cattran, D.; Roberts Ian, SD.; Troyanov, S.; Camilla, R.; Cook, T.; Feehally, J. (Jul 2010). "The new Oxford Clinico-Pathological Classification of IgA nephropathy.". Prilozi 31 (1): 241-8. PMID 20693944.
  39. ↑ 39.0 39.1 39.2 Fischer EG, Moore MJ, Lager DJ (October 2006). "Fabry disease: a morphologic study of 11 cases". Mod. Pathol. 19 (10): 1295-301. doi:10.1038/modpathol.3800634. PMID 16799480. http://www.nature.com/modpathol/journal/v19/n10/abs/3800634a.html.
  40. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 251. ISBN 978-1416002741.
  41. ↑ PS. April 2009.
  42. ↑ Epstein M, Oster JR, de Velasco RE (March 1976). "Hepatorenal syndrome following hemihepatectomy". Clin. Nephrol. 5 (3): 129-33. PMID 1261103.
  43. ↑ Angeli P, Merkel C (2008). "Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis". J. Hepatol. 48 Suppl 1: S93-103. doi:10.1016/j.jhep.2008.01.010. PMID 18304678.
  44. ↑ Wong F (February 2008). "Hepatorenal syndrome: current management". Curr Gastroenterol Rep 10 (1): 22-9. PMID 18417039.
  45. ↑ 45.0 45.1 http://emedicine.medscape.com/article/981126-overview
  46. ↑ AM. 13 August 2009.
  47. ↑ URL: http://www.kidneypathology.com/English_version/Amyloidosis_and_others.html. Accessed on: 9 November 2010.
  48. ↑ Racusen LC, Solez K, Colvin RB, et al. (February 1999). "The Banff 97 working classification of renal allograft pathology". Kidney Int. 55 (2): 713–23. doi:10.1046/j.1523-1755.1999.00299.x. PMID 9987096. http://www.nature.com/ki/journal/v55/n2/full/4490631a.html.
  49. ↑ Vascular deposition of complement-split products in kidney allografts with cell-mediated rejection. Feucht HE, Felber E, Gokel MJ, Hillebrand G, Nattermann U, Brockmeyer C, Held E, Riethmüller G, Land W, Albert E. Clin Exp Immunol. 1991 Dec;86(3):464-70. PMID 1747954.
  50. ↑ Impact of humoral alloreactivity early after transplantation on the long-term survival of renal allografts. Lederer SR, Kluth-Pepper B, Schneeberger H, Albert E, Land W, Feucht HE. Kidney Int. 2001 Jan;59(1):334-41. PMID 11135088.
  51. ↑ Mackenzie EF, Poulding JM, Harrison PR, Amer B (1978). "Human polyoma virus (HPV)--a significant pathogen in renal transplantation". Proc Eur Dial Transplant Assoc 15: 352–60. PMID 216990.
  52. ↑ 52.0 52.1 Nickeleit, Volker; Singh, Harsharan K. Polyomavirus Allograft Nephropathy: Clinico-Pathological Correlations. URL: http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=eurekah&part=A74503#A74539. Accessed on: 8 November 2010.
  53. ↑ Zarifian A, Meleg-Smith S, O'donovan R, Tesi RJ, Batuman V (June 1999). "Cyclosporine-associated thrombotic microangiopathy in renal allografts". Kidney Int. 55 (6): 2457–66. doi:10.1046/j.1523-1755.1999.00492.x. PMID 10354295.
  54. ↑ Fogo, Agnes; Bruijn, Jan A.; Cohen, Arthur H.; Colvin, Robert B.;Jennette, J. Charles (2006). Fundamentals of Renal Pathology (1st ed.). Springer. pp. 203. ISBN 978-0387311265.

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