Renal Function in Disease State Assessment of Renal Function Glomerular Filtration Rate (GFR) (Renal Failure → ↓ GFR) Estimation

of GFR is done from Plasma Urea Plasma Creatinine

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Disadvantage – Urea Production rate is production rate Proportional to affected by Skeletal Mass (Good if muscle mass • Protein Intake is constant) • Cell Catabolism Glomerular Filter (Leakiness of glomerular filter detected by) Proteinuria – Presence & Quality (the ↑ Damage to Glomerular Filter → ↑ Molecular Weight proteins leaked) Haematuria Examination of Urinary Deposits Tubular Function (not performed frequently, but valuable in) Acute Renal Failure (Acute Tubular Necrosis developed from Pre-Renal ARF) Defects of Renal Con centrating Ability Renal Tubular Acidosis

Creatinine Clearance Measurement “Steady State” depend on plasma [Creatinine] May be Normal until Creatinine Clearance dropped 50% Normal

Renal Failure Definition ↓ GFR – Impair Homeostatic Functions of Kidney Biochemical Features ↑ Plasma Urea, Creatinine Disturbed Na+, H2O balance (Water Retention → Dilutional HypoNatraemia) Acidosis (Fail to excrete Acid by Kidneys) K+ disturbances (Potassium Retention → HyperKalaemia) Ca2+, Phosphate disturbances • 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 (↓ Glomerular Filtration) (Hypovolaemia, ↓ BP) • Bladder Renal vasoconstriction Plasma Urea ↑ until • Urethra ↓ GFR new steady state is Caused by reached ↑ ADH • 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 ckLoss - H2O, Electrolyte diffusion of urea) (severe diarrhea) (Plasma Urea ↑ disproportionately Can progress to Intrinsic Renal Failure more than Plasma [Creatinine]) Can damage Kidney, Can damage Kidney, cause Renal Uraemia cause Renal Uraemia ↑ Urea Pro uc 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 ↑)

Renal Tubular Aci osis (RTA) Results from Ineffective Tubular Secretion of H+ Location of Defect, results in Proximal RTA Distal RTA Type II Type I Bicarbonate Ion Wasting Failure to Excrete daily metabolic load of acid Associate with other proximal tubular efects Phosphaturia Glycosuria Aminoaciduria (Fanconi syndrome ) Distal H+ secretory Able to Reabsorb Bicarbonate Ions in mechanisms is intact, Proximal Tubule patients are capable to Cannot Acidify Urine produce urine of ↓ pH Urine pH always > 5.3 (< 5.3) (under any circumstances ) (during severe acidosis) (even severe systemic acidosis) Features • Urine pH always > 5.3 • Chronic Hyperchloraemic Metabolic Acidosis Normal Anion gap • Vitamin D resistant rickets (caused by Chronic Acid osis) • Renal Calculi & Nephrocalcin osis (Ca2+ salts precipitate out more readily in constantly Alkaline urine) • Hypokalaemia (Defective Distal Tubular H+-Na+ ion exchange ) (↑ Urinary Na+ loss with consequent 2° Hyperaldosteronism)

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Acute Renal Failure (ARF) Occur over a short period (hours or days) Associated with Oliguria (urine output < 400ml/day) Causes of Oliguria (Results in Ischae mia, ↓ GFR, Tubular Dysfunction) Tubular Obstruction (due to cellular debris) Tubular Back Flow (Glomerular Filtrate Reabsorption) through damaged tubular epithelium Alterations in Renal Haemodynamics Causes of ARF Pre-Renal Renal Post-Renal Hypovolaemia Acute Tubular Necrosis Urinary Tract (Acute Ischaemic Re nal Failure) Obstruction ↓ CO Glomerulonephritis Nephrotoxins Drug Reactions 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 Urine Osmolality > 500 mmol/kg Urine Urea/ Plasma Usually > 10 Urea Ratio Urine [Na+] Usually < 20 mmol/L

Chronic Renal Failure (CRF) Develops over a long period of time (months to years) Destruction of Renal Parenchyma, ↓ Functional Nephron Mass Dietary load is too ↑ for Failing Kidney to excrete it, results in Sodium Retention (Hypertension, Edema) (50% Nor mal GFR ↓) Water Retention (HypoNatraemia) Potassium Retention (HyperKalaemia) (60% Normal GFR ↓) Anaemia (↓ Erythropoietin produced by Kidney) (60% Normal GFR ↓) Progressive Uraemia (80% Normal GFR ↓) H+ Total Excretion Impaired (due to ↓ renal capacity to form NH4+) Metabolic Acidosi s (present but severity remains stable, although urinary H+ excretion ↓) Buffering of H+ by Calcium Salts in Bone Demineralization of Bone (often occurs in CRF)

Acute Renal Failure < 400 mmol/kg Usually < 5 Usually > 40 mmol/L

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