Friday, March 13, 2009

Renal Fxn in Dz State

Renal disease

> Classify based on their affected component:
a) Glomerular
b) Tubular
c) Vascular
> In renal disease structural and functional interactions are closely related.

Renal failure

Renal failure maybe defined as a reduction in GFR sufficient to impair the homeostatic functions of the kidney.
> Acute renal failure : Sudden onset
> Chronic renal failure : Slow progressive loss of functional nephrons

Biochemical changes

1) Elevated plasma urea and creatinine blood levels.

2) Disturbed sodium and water balance:
> usually sodium and water retention with, if anything, water retention being greater leading to àdilutional hyponatraemia

3) Acidosis:
> caused by failure of excretion of the acid load normally excreted daily by the kidneysàmetabolic acidosis

4) Potassium disturbances:
> usually potassium retention leading toà hyperkalaemia

5) Calcium and phosphate disturbances
> usually phosphate retention.-àhyperphosphatemia
> hypocalcaemia
1. caused by:
2. acidosis reducing the level of protein-bound calcium in serum.
3. high phosphate level within renal tubular cells inhibits production of 1,25-dihydrocholecalciferol which will cause poor calcium absorption from the gut.

> hypocalcaemia will cause secondary hyperparathyroidism.
> in chronic renal failure, if these changes are not prevented, they lead to a metabolic bone disease called renal osteodystrophy

Other biochemical changes

6) Urate/uric acid retention
7) Secondary hyperlipidaemia
8) Magnesium retention -àhypermagnesemia

Acute renal failure(hours to days)

An acute onset of renal disease sufficiently severe to cause failure of renal homeostasis,rapid reversible decrease of GFR.
3 phases:
1) Oliguric(urine output<400/ml)>
1) Prerenal: sudden decrease in renal bld flow eg. Cardiac failure, hemorrhage burns/true volume depletion/hypotension
2) Renal/intrinsic: (1-tubulointerstitial,2-glomerular)
> Renal tissue damage eg. Acute tubular necrosis-
3) PostrenalObstruction to urine flow within the urinary system (BPH)

Chronic renal failure (>3 months)

Dysfunction that develops over a long period of time .

Disorder can be explained in terms of the destruction of renal parenchyma and the resultant decrease in functional nephron mass. Impaired in:
a) Ultrafiltration of plasma at glomerulus
b) Tubular reabsorption
c) Tubular secretion

Signs & Symptoms:
1) Sodium retention, leading to hypertension and perhaps oedema
2) Water retention, leading to hyponatraemia.
3) Potassium retention, leading to hyperkalaemia
4) Anaemia is a feature of CRF because of deficient erythropoetin production by the kidney
5) Progressive ‘uraemia’

Dialysis Indications (ARF)

1) Refractory hyperkalemia
2) Metabolic acidosis
3) Volume overload
4) Mental status changes

Hemodialysis Indications (CRF)

1) Uremia - azotemia with symptoms and/or signs
2) Severe Hyperkalemia
3) Volume Overload - usually with congestive heart failure (pulmonary edema)
4) Toxin Removal - ethylene glycol poisoning, theophylline overdose, etc.
5) An arterio-venous fistula in the arm is created surgically Catheters are inserted into the fistula for blood flow to dialysis machine

Glomerular disease

Causes is diverse:
1) Hereditary
2) Metabolic
3) Immunologic

Damage of the glomeruli
1) Affects GFR & membrane permeability
2) Most common immunological mediated
> Acute glomerulonephritis
> Chronic glomerulonephritis
> Nephrotic syndrome

Tubular disease

Affects tubular functions
1) Reducing tubular reabsorption & secretion of solutes
2) Ability to concentrate
3) Inherited @ induced
4) Renal tubular acidosis ~ distal & proximal type
> distal defect (RTA)~ unable to reabsorb bicarbonate ions in the proximal tubule
> cannot acidify the urine, i.e. urine pH is always greater than 5.3 , even during severe systemic acidosis

Assessment Of Renal Function

1) GFR(plasma urea,plasma creatinine,creatinine clearance measurement)
2) Glomerular filter- eg:leakiness in proteinuria,haematuria,urinary deposit)
3) Tubular function-not performed very frequently

Prepared by: Adam Al-Anas


ainaa ismail on March 16, 2009 at 10:03 AM said...

kenapa hyperNa?bukan hypo ke sebab Na tak dpt diserap?


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