Function of Kidney Excretion of waste products 2. Regulation of acid-base balance 3. Regulation of salt-water balance 4. Formation of renin and erythropoietin
Renal Function Tests
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.
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.
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.
CLINICAL FEATURES D epends 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.
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.
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
Lab findings
Complications of ARF
Chronic renal failure It is a syndrome characterized by progressive and irreversible deterioration of renal function due to slow destruction of renal parenchyma .
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.
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.
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.
CLINICAL FEATURES. Clinical manifestations of full-blown CRF explained by primary (renal) uraemic manifestations Secondary (systemic or extra-renal) uraemic manifestations.
Primary uraemic (renal) manifestations. 1. Metabolic acidosis. . 2. Hyperkalaemia 3. Sodium and water imbalance 4. Hyperuricaemia . 5. Azotaemia.
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
Lab findings in CRF Elevated BUN & creatinine Decreased GFR Hyperkalaemia Hyponatremia Acidosis Hypocalcaemia Hyperphosphatemia Elevated Uric acid Hypoproteinemia Anaemia Elevated cholesterol levels
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%
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
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