1. Renal failure can be acute or chronic and is classified based on the underlying cause and pathology. Acute renal failure (ARF) is characterized by a rapid decline in renal function and accumulation of waste products in the blood. Common causes of ARF include decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction. 2. Chronic renal failure (CRF) is an irreversible deterioration of renal function that develops slowly over time. It can be caused by diseases affecting the glomeruli or tubulointerstitial tissues. CRF results in fluid and electrolyte imbalances as well as metabolic abnormalities that manifest as uraemic symptoms. 3. Laboratory findings in renal

1. Renal failure

2. Nephron

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

4. Renal Function Tests

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

11. Lab findings

12. Complications of ARF

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

20. Lab findings in CRF
• Elevated BUN & creatinine
• Decreased GFR
• Hyperkalaemia
• Hyponatremia
• Acidosis
• Hypocalcaemia
• Hyperphosphatemia
• Elevated Uric acid
• Hypoproteinemia
• Anaemia
• Elevated cholesterol levels

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