KIDNEY - normal histology, clinical syndromes related to renal failure, Pathophysiology of renal failure, ARF

1. Kidney - normal histology, clinical syndromes related to
renal failure, Pathophysiology of renal failure, ARF

2. objectives
• Describe normal histology of kidney
• Define, classify and distinguish the clinical syndromes related to renal
failure
• Pathophysiology of renal failure
• Define and describe the etiology, precipitating factors, pathogenesis,
pathology, laboratory, urinary findings, progression and complication
of acute renal failure

3. anatomy
• Kidneys are bean shaped paired organs, weighing approx. 150 gm in
adult male and 130 gm in adult female
• Hilum is situated at mid point medially where the artery, vein,
lymphatics and ureter are located
• Kidney is surrounded by a thin fibrous capsule which is adherent at
the hilum.

4. Cut surface of kidney shows:
1.Renal cortex
2.Renal medulla
3.Renal pelvis
anatomy

5. • Cortex – peripheral – glomeruli and 85% nephron tubules.
- 15% nephrons consists of collecting tubules,
collecting duct, loops of Henle and vasa recta send their loops into the
medulla – juxta medullary nephrons.
• Medulla – inner – cone shaped renal pyramids
• Pelvis – innermost – funnel shaped collection area for drainage into
ureter. Minor calyces collect urine from renal papillae and drain into
major calyces.
anatomy

6. Histology
1. Renal vasculature
2. Glomerulus
3. Tubules

7. Renal vasculature

8. Renal vasculature

9. Nephron – longitudinal section

10. Renal cortex:
• 90% of the total blood supply
• Pressure in glomerular capillaries is high
• Renal cortex is more prone to be effected by HTN
Renal medulla:
• Poorly perfused
• Medullary necrosis

11. Glomerulus:
• Capillary tuft
• Podocytes
• Major function is complex filtration from capillaries
• Filtrate lacks protein and cells
• GFR is 125ml/minute
• 3 components:
1. Fenestrated endothelial cells
2. Glomerular basement membrane
3. Filtration slit pores

12. Glomerular filtration barrier

13. Structure of a nephron
• Glomerular capsule
• PCT
• Loop of Henle
• DCT
• Collecting ducts

14. Tubules
• Greatest amount of renal parenchyma
• Structure varies in different parts
1. PCT:
• First part, highly specialized, lined by cuboidal cells with brush
borders composed of microvilli
• It contains mitochondria, golgi apparatus, endoplasmic reticulum
• Major function – active reabsorption of filtered (Na, K, glucose, amino
acids, proteins, vitamins, bicarbonate, phosphate, calcium, and uric
acid. Passive reabsorption of 80% filtered water.

15. 2. Loop of Henle:
• PCT drains into the straight part of loop of Henle
• Thin descending, thin and thick ascending limbs
• The descending segment is lined by simple epithelium and ascending limb
is lined by columnar cells
• Active reabsorption of Na, K, Cl, and passive diffusion of water –
concentrated filtrate of urine
3. DCT:
• Transition from thick ascending limb where meets vascular pole of
glomerulus of its origin, to the early collecting ducts
• Epithelium is cuboidal
• Contributes to urine concentration and acidification
• Macula densa is a source of renin and has role in sodium metabolism

16. 4. Collecting ducts:
• Final pathway to reach tip of renal papilla
• Lining cells are cuboidal lacking brush borders
• Reabsorb water under ADH control and secrete H and K ions

17. Interstitium
• Cortical - scant, contains small number of fibroblast like cells
• Medullary – plentiful and contains stellate interstitial cells.
• It produce antihypertensive agents and are involved in metabolism of
prostaglandins

18. Renal function test
• Excretion of waste products
• Regulation of acid base balance
• Regulation of salt water balance
• Formation of renin and erythropoietin

19. Renal function tests

20. Urine analysis
• Physical examination
• Chemical tests
• Bacteriologic examination
• Microscopy

21. Concentration and dilution test
• To determine functional capacity of the renal tubules
• Depends upon activity of tubular cells in renal medulla and anti
diuretic hormone (ADH)
- defect in renal medulla (nephrogenic diabetes insipidus)
- lack of ADH (central diabetes insipidus).
• Specific gravity (remains constant in tubular disease)

22. Blood chemistry
Impaired renal function results in elevation of end product of protein
metabolism, chiefly:
• Urea
• BUN
• Creatinine
• Beta 2 macroglobulin – LMW protein – glomerular disease, increased
production

23. Renal clearance test
• Rate of glomerular filtration
• Normal = 120ml/minute in an average adult
C= UV/P
C= clearance of the substance in ml/minute, U= concentration of the
substance in urine, V= volume of urine passed per minute, P=
concentration of the substance in plasma.

24. Renal clearance tests
• Insulin or mannitol clearance test
• Creatinine clearance test
• Urea clearance test
• Para amino hippuric test (PAH)

25. Pathophysiology of renal failure
Glomerular diseases
• Most often immunologically-mediated
• Acute or chronic
Tubular diseases
• Caused by toxic or infectious agents likely
• Often acute
Interstitial diseases
• Due to toxic or infectious agents
• Involve interstitium and tubules
Vascular diseases
• Involves nephrons due to increased intraglomerular pressure ie:HTN,impaired blood flow

26. Acute renal failure (ARF)
Syndrome characterized by rapid onset of renal dysfunction
predominantly oliguria and sudden increase in metabolic waste
products

27. Etiopathogenesis of ARF
• Pre-renal causes
• Intra-renal causes
• Post-renal causes

28. Prerenal causes
Results in sudden decrease in blood flow to nephrons
Renal ischemia causing functional disorders or lowering GFR
Both
It causes
• Inadequate cardiac output
• Hypovolaemia
These result into reduced renal perfusion

29. Intra-renal causes
Disease of renal tissue itself
It includes
• Vascular and of arteries and arterioles
• Disease of glomeruli
• Acute tubular necrosis due to tubular ischemia or nephrotoxins
• Acute tubulointerstitial nephritis
• Pyelonephritis

30. Post renal causes
Caused by obstruction of flow of urine anywhere along the renal
tract distal to opening of collecting ducts
Due to:
• Mass within the lumen or from wall
• External compression along the lower urinary tract

31. Clinical features
Depend upon cause and stage of disease
1. Syndrome of acute nephritis
2. Syndrome of accompanying tubular pathology
3. Pre-renal syndrome

32. 1. Syndrome of acute nephritis
Accompanied with acute post streptococcal glomerulonephritis and
rapidly progressive glomerulonephritis
Renal dysfunction due to extensive proliferation of epithelial cells in
glomeruli and mild increase in glomerular permeability and decrease GFR
Features:
• Mild proteinuria, haematuria, oedema, and mild HTN
• Fluid retention due to diminished GFR and increased water and salt
reabsorption in distal nephrons

33. 2. Syndrome of accompanying tubular pathology
ARF is caused by destruction of tubular cells of the nephrons
Stages:
Oliguric phase
Diuretic phase
Recovery phase

34. Stages of syndrome accompanying tubular pathology
Oliguric phase:
• Lasts 7-10 days
• Urinary output <400ml/day
• Increased concentration of waste products - azotemia, metabolic acidosis,
hyperkalaemia, hypernatremia, pulmonary oedema
Diuretic phase:
• Improvement in urinary output with onset of healing of tubules
• Due to drawing of water and sodium by [preceding high levels of of ure and creatinine
• Urine is of low and fixed specific gravity
Recovery phase:
• Healing of tubular epithelial cells
• Upto one year with regaining normal tubular function

35. 3. Pre-renal syndrome
• Secondary to disorders with no glomerular or tubular damage
• In marginal ischemia caused by renal arterial obstruction,
hypovolemia, hypotension, cardiac insufficiency
• Decrease in GFR resulting into oliguria, azotemia, fluid retention and
oedema
• Nephrons retain ability to concentrate the glomerular filtrate

36. TAKE HOMEM MESSAGE
• AKI is a common and serious problem
• All AKI are not same/equal
• Diagnosis of AKI is often delayed
• Earlier recognition and treatment of AKI sequelae may improve
outcome.

37. Thankyou!