This document summarizes various types of renal failure including acute renal failure and chronic kidney disease. It discusses the etiology, pathogenesis and phases of acute tubular necrosis. It also covers chronic glomerulonephritis and specific conditions like membranous nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, IgA nephropathy, and diabetic nephropathy. The document provides details on urine analysis findings, histopathology techniques like immunofluorescence and electron microscopy in the evaluation of renal diseases.

1. RENAL FAILURE
DR. M.MOUNIKA
1ST YEAR PG
PATHOLOGY
MODERATOR:
DR KR. GOPALAKRISHNAN MD.,
READER OF PATHOLOGY

2. RENAL FAILURE
• It happens when the kidneys cannot remove the body’s
metabolic wastes or perform their regulatory function.
• It is a systemic disease and is a final common pathway
of many different kidney and urinary tract diseases.

3. ACUTE RENAL FAILURE
• Is a syndrome characterized by rapid onset of renal
dysfunction, chiefly oliguria or anuria, and sudden
increase in metabolic waste products [urea and
creatinine ] in the blood with consequent development
of uraemia.

4. ETIOPATHOGENESIS
A. PRERENAL
1. Hypovolemia.
2. Altered renal hemodynamics resulting in
hypoperfusion.
3. Inadequate cardiac output.

5. B. INTRARENAL
1. Vascular disease.
2. Diseases of the glomeruli.
3. Acute tubular necrosis.
4. Tubulointerstitial nephritis.
5. Pyelonephritis.
6. Nephrotoxicity.

6. C. POSTRENAL
1. Ureteric.
2. Bladder neck.
3. Urethra.

7. PHASES OF ACUTE TUBULAR
NECROSIS
3 PHASES:
1. Oliguric phase.
2. Diuretic phase.
3. Phase of recovery.
PRERENAL SYNDROME:

8. CHRONIC KIDNEY DISEASE
• Is a syndrome characterized by progressive and
irreversible deterioration of renal function due to slow
destruction of renal parenchyma, eventually
terminating in death when sufficient number of
nephrons have been damaged.

9. ETIOPATHOGENESIS
1. Glomerular pathology:
Primary -
Membranous glomerulonephritis
Membrano-proliferative glomerulonephritis.
Lipoid nephrosis.
Anti- glomerular basement membrane nephritis.
Systemic-
Systemic lupus erythematosus.
Diabetic nephropathy.

10. ETIOPATHOGENESIS CONT..
2. Tubulointerstitial pathology:
• Vascular causes.
• Infectious causes.
• Toxic causes.
• Obstructive causes

11. PATHOPHYSIOLOGY
Two mechanisms
• Initiating mechanisms specific to the underlying etiology.
•A set of progressive mechanisms, involving hyper-filtration
and hypertrophy of the remaining viable nephrons.
Stages of CRF: are based on the GFR.

12. STAGES OF CHRONIC RENAL FAILURE
• Decreased renal reserve.
• Renal insufficiency.
• Renal failure.
• End stage kidney[ chronic kidney disease]

13. PATHOGENESIS OF GLOMERULAR
INJURY
Immune mechanisms underlie most forms of primary
glomerulopathy and many of secondary glomerular
disorders.
• Antibody mediated
• Cell mediated
• Activation of alternative complement pathway.

14. ANTIBODY MEDIATED
Two mechanisms:
1. Antibodies reacting in situ within the glomerulus.
[fixed intrinsic tissue antigens, planted antigens]
1. Deposition of circulating antigen-antibody complexes
in the glomerulus. [exogenous and endogenous
antigens]

15. ACUTE TUBULAR NECROSIS
2 Types.
• Ischaemic ATN- shock, crush injuries, non-traumatic
rhabdomyolysis, mismatched blood transfusions, black
water fever.
• Toxic ATN- general poisons, heavy metals, drugs,
radiographic contrast material.

17. Nephritic syndrome:
It is a clinical syndrome characterized by:
• Hematuria with RBCs casts.
• Proteinuria (<3 gm).
• Hypertension.
• Mild edema.
• Oliguria.

18. PATHOGENESIS
• It is an acute glomerular injury. Lesions causing nephritic
syndrome have in common proliferation of endocapillary
cellularity (Mesangial and endothelial cells) and
associated with leukocytic infiltration. Inflammatory
reaction injures the capillary wall, permitting escape of
RBCs and proteins in urine (hematuria and proteinuria). At
the same time increased Mesangial cellularity compress
capillary Lumina and inducing hemodynamic changes that
lead to reduction of GFR that manifested clinically by
oliguria with fluid retention and azotemia.
• Hypertension results from fluid retention and renin
release from such ischemic kidney.

20. Rapidly progressive glomerulonephritis
[RPGN]
• Presents with an acute reduction in renal function
resulting in acute renal failure in a few weeks or
months.
• It is characterized by formation of crescents outside
the glomerular capillaries.

21. PATHOGENESIS
• Injury of capillary wall leads to escape of plasma
proteins, fibrin and inflammatory cells to Bowman's
capsule.
• This will lead to proliferation of parietal cells with
infiltration of macrophages and interstitial fibroblasts
leading to crescent formation.
• Crescents eventually obliterate Bowman's space and
compress the glomeruli.

22. TYPES
Type 1 RPGN: anti-GBM nephritis
Type 2 RPGN: any immune complex GN may lead to RPGN.
Type 3 RPGN: pauci-immune

24. CHRONIC GLOMERULONEPHRITIS:
• It is the end-stage of a variety of glomerular diseases
which result in irreversible impairment of renal
functions.
• It constitutes 35-50% of end-stage renal disease that
require chronic dialysis or renal transplantation.

25. FOCAL SEGMENTAL
GLOMERULOSCLEROSIS (FSGS)
• Characterized histologically by: focal and segmental
obliteration of capillary loops by increased collagen
(sclerosis) and accumulation of lipid and proteinaceous
material
Types:
• Idiopathic.
• Superimposed with primary glomerular disease.
• Secondary.

26. PATHOGENESIS
• Injury to visceral epithelial cells is its hallmark that
leads to focal hyper-permeable foci leading to
entrapment of plasma proteins and lipids. This results
into mesangial cell reaction with increased mesangial
matrix.

28. MEMBRANOUS NEPHROPATHY
• Diffuse thickening of the glomerular capillary wall due
to the accumulation of deposits containing Ig along the
subepithelial side of the basement membrane.
• 75% primary and remaining secondary.
• Drugs[penicillamine, gold, captopril, NSAIDS],
underlying malignant tumours, SLE, infections,
autoimmune disorders.
• Chronic immune complex mediated disease.

30. MEMBRANOPROLIFERATIVE
GLOMERULONEPHRITIS
• Immune mediated injury rather than a specific
disease.[hepatitis C and B]
• 2 types
Pathogenesis:
• Evidence of immune complex in the glomerulus and
activation of both classical and alternative complement
pathways.

32. DIABETIC NEPHROPATHY
• Glomerular lesions.
1. Capillary basement membrane thickening.
2. Diffuse mesangial sclerosis.
3. Nodular glomerulosclerosis.
• Renal vascular lesions.
1. Renal atherosclerosis and arteriosclerosis.
• Pyelonephritis.

33. DIABETIC NEPHROPATHY

34. IGA NEPHROPATHY/BERGER DISEASE
Etiopathogenesis:
• Hereditary or acquired[respiratory or gastrointestinal
exposure to environmental antigens] defect leading to
aberrantly glycosylated IgA1 which form immune
complexes deposited in the mesangium.

35. IMMUNOFLUORESCENCE
LOCATION:
• Subendothelial deposit.
• Subepithelial deposit.
• Intramembranous deposit.
• Mesangial deposit.
STAINING PATTERN:
• Diffuse linear staining.
• Granular lumpy bumpy deposits.
• Irregular fluffy deposits.

36. ELECTRON MICROSCOPY
• Effacement of podocytes.
• Electron dense immune complex.
• GBM thickening.
• GBM replication.
• Collagen matrix deposition.
• Fibrillary deposit.

37. URINE ANALYSIS
Pre-renal ARF:
• Specific gravity>1.018.
• Hyaline casts.
Intrinsic ARF:
1. Renal artery thrombosis:
• Mild proteinuria.
• Occasional hematuria.

38. 2. Athero-embolic disease:
• Eosinophiluria.
3. Renal vein thrombosis:
• Mild proteinuria.
• Occasional hematuria.
4. Glomerulonephritis/ vasculitis:
• Hematuria with red cell casts/ dysmorphic red cells.
• Granular casts.
• Proteinuria [<1g/dl]

39. 5. Hemolytic-uremic syndrome/ thrombotic
thrombocytopenic purpura:
• Hematuria.
• Mild proteinuria.
• Red cell casts[rare].
6. Malignant hypertension.
• Hematuria with red cell casts/ proteinuria.
7. Acute tubular necrosis:
• Muddy brown granular or tubular epithelial cell casts.
• Specific gravity<1.015.

40. 8. Allergic interstitial nephritis:
• White cell casts.
• Eosinophiluria.
9. Acute bilateral pyelonephritis:
• Leucocytes.
• Proteinuia.
• Positive urine culture
Postrenal ARF:
• Usually normal.
• Hematuria if due to stones.

41. CHRONIC GLOMERULONEPHRITIS
• Fixed specific gravity.
• Proteinuria
• Waxy casts

43. HEMOTOLOGY

44. THANK YOU