Renal function

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Renal Function Concept

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Renal function

  1. 1. RENAL FUNCTION1. MAINTENANCE OF WATER AND ELECTROLYTE BALANCE OF THE BODYThe proximal renal tubules reabsorb about 85% of water filtered by the glomerulus, while the restpasses through the loop of Henle where some of the water is reabsorbed.The cell lining the collecting ducts which are normally impermeable to water are rendered permeable bythe action of an antidiuretic hormone (ADH, vasopressin). Thus, water is allowed to re-enter circulation.When the body needs to excrete more water, resulting in more water being excreted in the urine (diluteurine).2. MAINTENANCE OF BLOOD PHSubstances that cause the pH of blood to rise or fall are removed by the kidneys. Substances of acidreaction are waste products of protein metabolism-urea, uric acid and creatinine.3. EXCRETIONWaste products of drugs which are left in the body are later on excreted via kidneys. Toxic substanceswhich are rendered harmless in the liver are excreted by the kidneys in the urine.4. FILTRATIONThe glomerular filtration rate (GFR) measures the efficiency of this filtration and it is determined by ureaand creatinine clearance tests. The filtrate passes from the Bowman’s capsule into the renal tubule.During this passage, the tubular cells reabsorb those substances that are needed by the body into thebloodstream.5. PRODUCTION OF ERYTHROPOEITINThe substance that is necessary for the normal production of rbc in the bone marrow is theerythropoietin. It is produced by the kidneys.6. REABSORPTIONDesirable elements in the filtrate such as glucose and amino acids are reabsorbed. This reabsorptionoccurs mainly in the proximal convulated tubules.AETIOLOGY - Acute renal failure (ARF)-the kidneys fail over a period of hours or days. May be reversed and normal renal function regained. - Chronic Renal Failure (CRF)-develops over months or years and leads eventually to end stage of renal failure (ESRF). Irreversible.ARF • Sudden deterioration of renal function indicated by rapid rising of serum urea and creatinine concentration.Kidney failure can be classified as: -Pre-renal : the kidney fails to receive a proper blood supply -Post-renal : the urinary drainage of the kidney is impaired because of an obstruction.
  2. 2. -Renal : intrinsic damage to the kidney tissue. This may be due to a variety of diseases, or the renal damage may be a consequence of prolonged pre-renal or post-renal problems.DIAGNOSIS  Decreased plasma volume because of blood loss, burns, prolonged vomiting or diarrhea  Diminished cardiac output  Local factors, such as occlusion of renal arteryBIOCHEMICAL FINDINGS  Serum urea and creatinine are increased  Metabolic acidosis  Hyperkalaemia  A high urine osmolality Post-renal factor: filtration at the glomeruli is reduced caused by blockage e.g; renal stones, carcinoma of cervix, prostate or occasionally bladderACUTE TUBULAR NECROSIS  Acute blood loss in severe trauma  Septic shock  Specific renal disease- glomerulonephritisMANAGEMENT  Correction of pre-renal factors, if present, by replacement of any ECF volume deficit.  Treatment of underlying disease  Biochemical monitoring  DialysisConsequences of CRFSodium and water metabolism  Retain ability to reabsorb sodium  Or renal tubules may loose ability to reabsorb water and there for urine is concentrated.Potassium metabolism  Sudden deterioration of renal function may precipitate a rapid rise in serum potassium concentration.Acid-base balance  Retention of hydrogen ions-metabolic acidosis
  3. 3. Calcium and phosphate metabolism  The ability of renal cells to make vitamin D decrease  Calcium absorption is reduced-hypercalcemia  Parathyroid hormone is stimulated in a attempt to restore plasma calcium to normal, but adverse effects of renal osteodystrophyErythropoietin synthesis  Normochromic normocytic anaemia is due to failure of erythropoietin production.  Biosynthesized human erythropoietin may be used to treat the anaemia of CRF.Management  Water and sodium intake should be carefully matched to the losses.  Hyperkalaemia may be controlled by oral ion-exchange resins (resonium A).  Hyperphosphataemia may be controlled by oral aluminium or magnesium salts  The administration of hydroxylated vitamin D metabolites may prevent the development of secondary hyperparathyroidism.  Dietary restriction of protein, to reduce the formation of nitrogenous waste product.  Dialysis & renal transplantRENAL FUNCTION TESTSUREAUrea is carried by the plasma to the kidney where it is filtered from the plasma by the glomerulus. About40% of the urea in the glomerular filtrate is reabsorbed by the renal tubules.ESTIMATION OF UREANormal range of blood ureaAdults: 2.5-7.0 mmol/L (15-40 mg/dl)Excess of urea in blood- uraemiaResult of kidney impairmentUrea clearance testSample: 24 hour urine specimen & blood sampleNormal range: 40-65 ml/min< 10 ml/min during renal failureCREATININEA nitrogenous product which is produce from the metabolism of creatinine from the metabolism ofcreatine in skeletal muscles. It is filtered ion kidneys and excreted in the urine.
  4. 4. CREATININE CLEARANCE TESTSample: 24 hour urine specimen & blood sampleNormal range for creatinine serum/plasmaAdult men 88-135 umol/LAdult female 62-115 umol/LCreatinine clearanceAdult men 97-137 ml/minAdult female 88-128 ml/minHigh serum or plasma creatinine levels- kidney impairment Creatinine clearance is calculated from the formula: U urinary creatinine concentration (μmol/L) V urine flow rate (mL/min i.e., 24hr urine volume(ml)divided by 1440(min)) P plasma creatinine concentration (μmol/L)URIC ACIDUric acid is the final breakdown product of purine metabolism.Converted in liver into uric acid and filtered in kidney.Nearly all of the uric acid in plasma is in the form of monosodium urate- insolubleAt high levels (> 6.4 mg/dl), the plasma is saturated; urate crystals may form and precipitate in tissuesNormal range:Adult males: 3.5-7.2 mg/dlAdult female: 2.6-6.0 mg/dlGout is an arthropathy caused by the precipitation of monosodium urate crystals in synovial joints. Thisoccurs when plasma urate concentrations are elevated. Secondary causes of hyperuricaemia includerenal disease, thiazide diuretics, increased cell turnover and a high intake of purine-rich foods. Gout andhyperuricaemia show a strong familial incidence. Some very rare inherited defects in purine metabolismthat cause hyperuricaemia have been described, but in the majority of patients, there is no such defect,and hyperuricaemia is thought to be due to decreased renal urate excretion. Gout usually presents as anacute arthritis, but can lead to chronic joint disease, and crystals of monosodium urate can be depositedin tissues and in the renal tubules, causing an obstructive uropathy.
  5. 5. URINARY CALCULIAbnormal, solid concentration of mineral and salts performed around organic materials and foundchiefly in ducts and cysts. The presence of calculi in the urinary tract can obstruct urinary flow, and cancause infection and haematuria.Kidney calculi –hydronephrosisCalculi found in ureter- causing pain and bleeding.Type frequency morphologyCalcium oxalate 70% Rough, small,Phosphate calculi 15% Soft, grayish-white,bigUric acid 10% Rough, small, yellowish-brownCystine and xantin rare Soft, small, round,yellowish, contains fatURINE OSMOLALITYFirst and most important crucial test is to determine urinary osmolality by osmometer.Normal urine osmolalityOsmotic limits- 50 to 1200 mosm/kg< 200 mosm/kg –water diuresisPossibilities are following:-psychogenic polydipsia (compulsive water drinking)-central diabetes insipidus (HDI)The above two conditions are differentiated by either: a) Water deprivation test by attempting to elicit ADH secretion by water deprivation. b) DDAVP test administration of DDAVP, renal conservation of water occursREFERENCE:Allan, G. & Michael, J.M. 2005. Clinical Biochemistry. 3rd Ed. London: Churchill Livingstone.Marshall, J.W. & Bangert, S.K. 2008. Clinical Chemistry. 6th Ed. London: Mosby Elsevier.Ochei, J. & Kolhatkar, A. 2006. Medical Laboratory Science. 4th Ed. New Delhi: Tata McGraw-Hill.

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