Assessment of Renal Function Renal Tubular Acidosis (RTA)
Glomerular Filtration Rate (GFR) Results from Ineffective Tubular Secretion of H+ (Renal Failure → ↓ GFR) Location of Defect, results in Estimation of GFR is done from Proximal RTA Distal RTA Plasma Urea Plasma Creatinine Creatinine Clearance Type II Type I Measurement Bicarbonate Ion Wasting Failure to Excrete daily metabolic load of acid Disadvantage – Urea Production rate is “Steady State” depend Associated with other production rate Proportional to on plasma [Creatinine] proximal tubular defects affected by Skeletal Mass May be Normal until Phosphaturia • Protein Intake (Good if muscle mass Creatinine Clearance Glycosuria • Cell Catabolism is constant) dropped 50% Normal Aminoaciduria Glomerular Filter (Fanconi syndrome ) (Leakiness of glomerular filter detected by) Distal H+ secretory Able to Reabsorb Bicarbonate Ions in Proteinuria – Presence & Quality mechanisms is intact, Proximal Tubule (the ↑ Damage to Glomerular Filter → ↑ Molecular Weight proteins leaked) patients are capable to Cannot Acidify Urine Haematuria produce urine of ↓ pH Urine pH always > 5.3 Examination of Urinary Deposits (< 5.3) (under any circumstances ) Tubular Function (not performed frequently, but valuable in) (during severe acidosis) (even severe systemic acidosis) Acute Renal Failure (Acute Tubular Necrosis developed from Pre-Renal ARF) Features Defects of Renal Con centrating Ability • Urine pH always > 5.3 Renal Tubular Acidosis • Chronic Hyperchloraemic Metabolic Acidosis Normal Anion gap Renal Failure • Vitamin D resistant rickets Definition (caused by Chronic Acid osis) ↓ GFR – Impair Homeostatic Functions of Kidney • Renal Calculi & Nephrocalcin osis Biochemical Features (Ca2+ salts precipitate out more readily ↑ Plasma Urea, Creatinine in constantly Alkaline urine) Disturbed Na+, H2O balance (Water Retention → Dilutional HypoNatraemia) • Hypokalaemia (Defective Distal Tubular Acidosis (Fail to excrete Acid by Kidneys) H+-Na+ ion exchange ) K+ disturbances (Potassium Retention → HyperKalaemia) (↑ Urinary Na+ loss with consequent Ca2+, Phosphate disturbances 2° Hyperaldosteronism) • Phosphate Retention (↑ Phosp hate → Inhibit production of 1,25 -DHCC → ↓ GIT Ca2+ absorb) • HypoCalcaemia (Acidosis → ↓Protein-b ound Ca2+ in serum) (In Chronic Renal Failure, if not prevented, can lead to Metabolic Bone Disease – Renal Osteodystrophy) Urate Retention 2° Hyperlipidaemia Magnesium Retention (HyperMagnesaemia) Plasma Urea Urea formed in Liver (from Ammonia – released by deamination of amino acid) 75% of Non-Protein Nitrogen is Excreted as Urea (mainly by Kidneys) Small amounts loss through Skin, GIT Causes of ↑ Plasma Urea Pre-Renal Uraemia Renal Uraemia Post-Renal Uraemia Impaired renal Acute Renal Failure Outflow Obstruction perfusion Chronic Renal Failure • Ureter (Hypovolaemia, ↓ BP) (↓ Glomerular Filtration) • Bladder Renal vasoconstriction Plasma Urea ↑ until • Urethra ↓ GFR new steady state is Caused by ↑ ADH reached • Renal stones RAAS activation (Urea Production = • Prostatism (↑ Passive Tubular Excretion) • GU cancer Reabsorption of Urea) Shock Plasma Urea continue Back Pressure on Burns to ↑ in Near-Total Renal Tubules Haemorrhage Renal Failure (enhances ba ck- Loss - H2O, Electrolyte diffusion of urea) (severe diarrhea) (Plasma Urea ↑ Can progress to disproportionately Intrinsic Renal Failure more than Plasma [Creatinine]) Can damage Kidney, Can damage Kidney, cause Renal Uraemia cause Renal Uraemia ↑ Urea Produc#on ↑ Protein Intake ↑ Protein Catabolism • Trauma • Major Surgery • Starvation Haemorrhage in GIT (protein-meal blood ) Plasma Urea ↑ more than Creatinine (Tubular reabsorption of Urea is ↑) jslum.com | Medicine
Occur over a short period (hours or days) Develops over a long period of time (months to years) Associated with Oliguria (urine output < 400ml/day) Destruction of Renal Parenchyma, ↓ Functional Nephron Mass Causes of Oliguria (Results in Ischae mia, ↓ GFR, Tubular Dysfunction) Dietary load is too ↑ for Failing Kidney to excrete it, results in Tubular Obstruction (due to cellular debris) Sodium Retention (Hypertension, Edema) (50% Nor mal GFR ↓) Tubular Back Flow Water Retention (HypoNatraemia) (Glomerular Filtrate Reabsorption) through damaged tubular epithelium Potassium Retention (HyperKalaemia) (60% Normal GFR ↓) Alterations in Renal Haemodynamics Anaemia (↓ Erythropoietin produced by Kidney) (60% Normal GFR ↓) Causes of ARF Progressive Uraemia (80% Normal GFR ↓) Pre-Renal Renal Post-Renal H+ Total Excretion Impaired (due to ↓ renal capacity to form NH4+) Hypovolaemia Acute Tubular Necrosis Urinary Tract (Acute Ischaemic Re nal Failure) Obstruction Metabolic Acidosi s ↓ CO Glomerulonephritis (present but severity remains stable, although urinary H+ excretion ↓) Nephrotoxins Buffering of H+ by Calcium Salts in Bone Drug Reactions Demineralization of Bone (often occurs in CRF) Disorders of Renal Vasculature Renal Tubule Blockage Chemical Pathology of ARF Phases – Oliguric, Diuretic, Recovery Proteinuria present Urine dark (Haem pigments from Blood) Retention of Urea, Creatinine, Phosphate, Sulphate, other waste products in blood Renal Failure due to Trauma (including Surgical Operations), Plasma Urea ↑ more rapidly than Renal Failure due to Medical causes (Acute Glomerular Nephritis) Phases Oliguric Diuretic <400 mL urine / day (due to ↓ GFR) ↑ Losses of Electrolytes – Urine Urine Osmolality similar to Plasma Need to be replaced ↑ Urine [Na] (Orally/ Parenterally) Plasma Na ↓ due to Assess Urine Water Intake ↑, Excretion ↓ [Sodium] ↑ Metabolic Water [Potassium] (from ↑ Tissue Catabolism) Calculate daily output/loss Na+ Shift from ECF → ICF Plasma K+ ↑ due to Monitor Plasma Impaired Renal Output [Creatinine] ↑ Tissue Catabolism [Urea] Shift of K+ out of cells [Potassium] (Accompanied Metabolic Acidosis – developed due to Failure to excrete H+ ↑H+ formed from Tissue Catabolism)
Investigation of ↓ Urinary Output
Simple Hypovolaemia Acute Renal Failure Urine Osmolality > 500 mmol/kg < 400 mmol/kg Urine Urea/ Plasma Usually > 10 Usually < 5 Urea Ratio Urine [Na+] Usually < 20 mmol/L Usually > 40 mmol/L