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Acute Renal Failure

• ARF is the condition when kidney suddenly fails to excrete water,electrolytes & waste products.

Causes of ARF
• Acute nephritis- immune complex • Damage to renal tissue by poisons like lead,mercury & carbon-tetrachloride • Renal ischemia which is developed during ciculatory shock • Severe transfusions reactions • Sudden fall in B.P. during haemorrhage,dirrhoea,severe burn,cholera • Blockage of ureter due to formation of calculi

• Volume of urine out put is reduced (oligouria) & in severe condition –Anuria(stopage of urine formation) • Proteins +++ urine(proteinuria)-albumin++ • RBC,WBC & casts +++urine • Retention of Na & water- edema, ECFV • Hypertension • Acidosis • If the Patient is not treated in time ,the acidosis becomes severe resulting in coma & death within 10 to 15 days

Chronic Renal Failure
• When some of the nephrons loose function the unaffected nephrons can perform the functions. • However when more & more nephrons starts loosing the function over the months or years,the CRF is developed

Causes of CRF
• • • • • • Chronic nephritis Hypertension Renal stones Development of cyst in kidney Atherosclerosis Slow poisoning

• Excessive accumulation of metabolic end products like urea,creatinine in blood is called Uremia. • Common features of uremia are • Loss of appetite(anorexia) ,Lethargy • Drowsiness ,Nausea& vomiting • Pigmentation of skin,mascular twiching • Convulsions,confusion & mental deterioration

• • • • •

Acidosis Hyperkalemia Edema Anemia Hyperparathyroidism-is developed due to deficiency of 1,25 di-OHCCF.This causes removal of calcium from bones causing osteomalacia

• In physiologic sense refers to diffussion of solutes from an area of higher conc. To the area of lower conc.through a semipermeable membrane. • This principal has been used to dialyse the blood of patients with renal failure specially those developing Uremia. • Uremia develops>70% nephrons damaged

• Intermittent dialysis may prolonge the life of many patients with CRF. • it can partially replace excretory function of the kidneys but does not replace endocrine & metabolic functions


1) Excretory – primary :by urine formation 2) Regulation of volume & electrolyte composition of ECF 3) Regulation of acid-base balance 4) Endocrine function – produce & secrete: erythropoietin, renin, calcitriol(1,25-DHCC) 5) Site of neoglucogenesis – not primary: in starvations- esp. from glutamine

Renal Function Tests :

collective term for a variety of individual tests and procedures that can be done to evaluate how well the kidneys are functioning.
Practically, divided into 3 groups – 1) Analysis of urine & blood 2) Specific assessment of renal clearance 3) Additional special Tests

 Early detection of possible renal damage & assessment of its severity  Measure progression of the renal impairment & efficacy of corrective therapy  Predict when renal replacement therapy may be necessary  Monitor safe & effective use of drugs, which are principally eliminated through urine.

1)Volume 1000-2500 ml/d Normal  Polyuria >2.5L/d Chronic GN  Oliguria<400ml/d seen in Ac GN, Terminal RF • Anuria <100ml/d seen in Renal Failure

2) Appearance > clear  Turbid (alkalinity d/t prolonged standing l/t ppt of Ca/Mgphosphates,↑phosphate , presence of pus d/t UTI)
3) Colour> straw/amber-yellow urochrome Brownish yellow (jaundice) Dark (alkaptonuria) Reddish brown (RBC/Hb/Mb-uria,Porphyria etc.)

4) Odour> mild aromatic  volatile org. acids  Unpleasant ammoniacal (prolonged standing)  Acidotic fruity (DKA)

5) Sp. Gravivity & Osmolality >
 1.003 to 1.030 & 50-1200 mOsm/kg (depends on state of hydration of the body)  Early morning urine sample(=after overnight fast)if SG>1.018 & Osm>600 ≡Normal  SG is simplest to measure but unreliable(in presence of HMW substances) for evaluating renal concentrating ability.  SG  decreased,increased & fixed(1.010=CRF)

Applied aspect
• 12 hr water deprivation results in S.G. of urine to become 1025 with 1000 osmolarity. Failure to do this indicate abnormal renal functioning • in S.G. is seen in = • low water intake, DM, Albuminuria,Ac Nephritis • In S.G. is seen in= • Tubular Damage, Absence of ADH

B) BIOCHEMICAL : 1) Reaction > mild acidic  pH avg.6
(=4.5-7.5)  normal short PP alkaline tide  Protein rich diet  acidic  Vegetable rich diet  alkaline also in type II DTA, UTI by urease producing organisms, Acetazolamide therapy, alkali ingestion.

2) For abnormal urinary constituents : I) Proteins >
 Normal upto 150 mg/d—routinely undetected  Proteinuria >150mg/d albumin predominates  Glomerulonephritis, Pyelonephritis,Toxaemia of pregnancy, tubulo-interstial disorders

II) Reducing Sugars >
 Normally absent – glucose/fructose/galactose ++ DM,Renal Glycosuria,Alimentary Glycosuria Fructose,Galactose++in Metabolic disorders

III) Blood >Haematuria
 Normally does not appear  ++ Ac GN,Renal stones,Malignancy of UT

IV) Ketone Bodies >
 Normally not present
 ++Prolonged starvation,Diabetic Ketoacidosis

V) Bile salts >
 Only in early phases of obstructive jaundice  By- Hay’s test & Petenkoffer’s test

VI) Urobilinogen > N ~1 - 3.5 mg/d
 ↑ in persistent fevers, hepatobiliary diseases, haemolytic jaundice

VII) Bile-pigments >
 Bilirubinuria=↑conj.Bilirubin  hep/post-hep jaun  VIII) Haemoglobinuria
 Normally =absent  ++indicate intravascular Haemolysis(Black water fever due to falciperum malaria)

Imp findings in the urinary sediment includes---

I) Casts >>
  

proteinaceous plugs

Formation favoured by sluggish flow Various shapes c/t tubules in which formed cellular or non-cellular Types  Hyaline, RBC, WBC, Granular, Broad waxy etc.

II) Crystals >>
 Ca-oxalate/phosphate, Triple phosphate-common  May be normally found  risk of stone in future  Urate or Cysteine crystals  pathologic

III) Cells >>
 RBCs, WBCs, pus cells, Sq.epithelial, Tubular epithelial cells

ANALYSIS of Blood :
 There is no plasma constituent whose conc. depends solely on the functionality of kidneys.  Frequently used are 2 normal metabolic wastes  Excreted by kidneys  accumulates in renal dysfunction  ↑blood levels I) Blood Urea = 20-40 mg%  begin to rise only after 50% renal damage II) Plasma Creatinine >> 0.6 – 1.5 mg%  More reliable as blood ureaq is subjected to variations • Serum K+ =5mEq/L increased in oligoruria

Renal clearance TESTS:
Vol. of plasma that is cleared of a substance in unit time, by its’ urinary excretion ml/min Calculated as: C = UV/P Predominantly determine GFR: Relationship as— GFR = C No reabs, No Secret INULIN

Much reabs, No Secret
No reabs, Much Secret

Gluc, AA, Na+, ClPAH, Diodrast

Renal clearance TESTS:
• Correlated more directly with the status of kidney function  employed to assess GFR,RPF & RBF

Various markers used : A) Exogenous >> 1) Inulin (gold standard but technically demanding) 2) Non-radiolabelled contrast media (e.g. Iohexol) 3) Radiolabelled compounds (e.g. 99m TcDTPA) B) Endogenous >> 1) Creatinine (marginally overestimates— most widely used in clinical practice) 2) Urea (one of the 1st markers– not used at present)

** Prediction of GFR from Plasma creatinine levels:
 Approximation of bedside GFR with limited accuracy by ―Cockroft & Gault formula‖  Most widely used & best validated for adults Ccr =(140-Age)x(Wt in Kg)/(Plasma Creatinine x72)  [Correction factor for females = 0.85] value to such formulas for GFR prediction is likely to increase when an accurate plasma creatinine assay is performed along with inhibition of tubular secretion by cimetidine/probenecid.

Renal Imaging studies >>
Plain radiograph of abdomen IVP USG, CT Scan, MRI Scan Radionuclide studies Strictly speaking, these are not considered to be RFTs, but very useful in present day clinical practice for structural & functional assessment of kidneys.