3. Function of Kidney
1. Excretion of waste products
2. Regulation of acid-base balance
3. Regulation of salt-water balance
4. Formation of renin and erythropoietin
5. PATHOPHYSIOLOGY OF RENAL DISEASE:
• RENAL FAILURE
divided into 4 major groups
1. Glomerular diseases: immunologically-mediated- acute or chronic.
2. Tubular diseases: Toxic or infectious agents, acute.
3. Interstitial diseases: Toxic or infectious agents
4. Vascular diseases: Hypertension or impaired blood flow.
6. Acute Renal Failure (ARF)
It is a syndrome characterised by rapid onset of renal dysfunction, chiefly oliguria
or anuria, and sudden increase in metabolic waste-products in the blood with
consequent development of uraemia.
7. Pathogenesis
• Prerenal- cause sudden decrease in blood flow to the nephron.
Renal ischaemia,cardiac output and hypovolaemia.
• Intra Renal- disease of renal tissue itself.
vascular disease, diseases of glomeruli, acute tubular necrosis
• Post renal-obstruction to the flow of urine anywhere along the renal tract
distal to the opening of the collecting ducts.
8. CLINICAL FEATURES
• Depends on underlying cause and stage of the disease.
3 major patterns
• 1. Syndrome of acute nephritis- acute post-streptococcal glomerulonephritis,
rapidly progressive glomerulonephritis
• mild proteinuria, haematuria, oedema and mild hypertension.
9. 2. Syndrome accompanying tubular pathology
• destruction of the tubular cells of the nephron
i) Oliguric phase-7 to 10 days is characterised by output <400 ml/day, low
Specific gravity
• ii) Diuretic phase- healing of tubules, leads to improvement in urinary output
urine is of low or fixed specific gravity
• iii) Phase of recovery-Full healing in about half the cases, while others
terminate to death.
10. • 3. Pre-renal syndrome
• Occurs in marginal ischaemia caused by renal arterial obstruction,
hypovolaemia, hypotension or cardiac insufficiency.
Symptoms
• Oliguria
• Azotaemia (elevation of BUN and creatinine)
• Oedema
13. Chronic renal failure
• It is a syndrome characterised by progressive and irreversible deterioration of
renal function due to slow destruction of renal parenchyma.
14. ETIOPATHOGENESIS
Diseases leading to CRF classified into 2 major groups:
• causing glomerular pathology,
• causing tubulointerstitial pathology.
• In the final stage of CRF, all parts of the nephron are involved.
15. • 1. Diseases causing glomerular pathology.
• Glomerular destruction results in changes in filtration process and leads to
development of the nephrotic syndrome characterised by
• proteinuria, hypoalbuminaemia and oedema.
Examples
• i) Primary glomerular pathology- various types of glomerulonephritis
• ii) Systemic glomerular pathology: systemic lupus erythematosus, serum
sickness nephritis and diabetic nephropathy.
16. 2. Diseases causing tubulointerstitial pathology.
• Cause alterations in reabsorption and secretion of important
constituents.
According to initiating etiology categorized into 4 groups:
• Vascular,
• Infectious,
• Toxic
• Obstructive.
17. CLINICAL FEATURES.
Clinical manifestations of fullblown CRF explained by
• primary (renal) uraemic manifestations
• Secondary (systemic or extra-renal) uraemic manifestations.
18. A. Primary uraemic (renal) manifestations.
1. Metabolic acidosis..
2. Hyperkalaemia
3. Sodium and water imbalance
4. Hyperuricaemia.
5. Azotaemia.
19. B. Secondary uraemic (extra-renal) manifestations.
1. Anaemia.
2. Integumentary system: Deposit of urinary pigment urochrome
3. Cardiovascular system. Increased workload, congestive heart failure.
4. Respiratory system: pulmonary congestion, pulmonary oedema
5. Digestive system: Anaemia, Gastrointestinal irritation
6. Skeletal system. Renal osteodystrophy
• Two major types of skeletal disorders may occur:
• i) Osteomalacia
• ii) Osteitis fibrosa occurs due to elevated levels of parathormone
21. Complications
1. Decreased renal reserve.
• Damage to renal parenchyma is marginal and the kidneys remain functional.
• GFR is about 50% of normal, BUN & creatinine- normal.
2.Renal insufficiency.
• 75% of destroyed. The GFR- 25%
3.Renal failure.
• 90% destroyed. GFR is approximately 10%
• Findings: oedema, metabolic acidosis, hypocalcaemia, and uraemia.
4.End-stage kidney. The GFR -5%
22. Questionarrie
• Define Renal failure
• Classify renal failure on etiological basis
• Define Acute Renal failure
• Discuss the etiopathogenesis of ARF
• Describe the pathology of ARF
• Enumerate the laboratory Findings in ARF
23. • Enumerate the clinical features and complications of ARF
• Renal function test
• Define Chronic Renal Failure
• Discuss the etiopathogenesis of CRF
• Describe the pathology of CRF
• Enumerate the lab findings in CRF
• Complication of CRF
Editor's Notes
of waste products resulting from protein
metabolism.
4 major groups according to the predominant involvement of corresponding morphologic components
Oliguric-metabolic acidosis, hyperkalaemia, hypernatraemia and hypervolaemia due to secondary effects of circulatory overload and pulmonary oedema.
