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Understanding Acute Renal Failure: Causes, Symptoms, and Recovery

Learn about the causes, symptoms, and recovery process of Acute Renal Failure (ARF), a condition characterized by a sudden reduction in renal function. Discover the different types of ARF, including prerenal, postrenal, and renal ARF, along with their specific causes. Understand the role of hemodynamic events and toxic effects in the development of ARF, and explore the changes that occur at the glomerular level. Find out how the renin-angiotensin system and endothelin concentration are involved in the pathophysiology of ARF.

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Understanding Acute Renal Failure: Causes, Symptoms, and Recovery

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  1. 1909 Starling: „The Kidney presents in the highest degree the phenomenon of sensibility… must be endowed with intelligence.” 1957 Homer-Smith: … only a passive agent operating blinly and automatically according to the dictates of receptor- effector systems located elsewhere in the body

  2. Acute Renal Failure (ARF) (an abrupt reduction in renal function) GFR Oliguric: urine output <500ml/day (70-80%) Non-oliguric: urine output >500 ml/day (20-30%) Changes inblood biochemistry ( accumulation of metabolic waste products; creatinin , urea , „azotemia” hyperkalemia, oedema, metabolic acidosis etc.) By the site of the abnormality Prerenal ARF or azotemia Postrenal ARF or azotemia Renal (parenchimal) ARF or azotemia (Acute tubular necrosis =ATN often used interchangeably with ARF

  3. Causes of Prerenal Azotemia Hypovolemia Hemorrhage Gastrointestinal losses Third space Pancreatitis Burns Peritonitis Traumatized tissue Diuretic abuse Impaired cardiac function Congestive heart failure Myocardial infarction Pericardial tamponade Acute pulmonary embolism Peripheral vasodilatation Bacteremia Antihypertensive medications Increased renal vascular resistance Anesthesia Surgical operation Hepatorenal syndrome Renal vascular obstruction, bilateral Embolism Thrombosis

  4. Causes of Postrenal Azotemia Obstruction of ureters, bilateral Extraureteral Tumor: cervix, prostate, endometriosis Periureteral fibrosis Accidental ureteral ligation during pelvic operation Intraureteral Sulfonamide and uric acid crystals Blood clots Pyogenic debris Stones Edema Papillary necrosis Bladder neck obstruction Prostatic hypertrophy Bladder carcinoma Bladder infection Functional: neuropathy or ganglionic blocking agents

  5. Specific Etiologies of Acute Renal Failure /1 I. Hemodynamic Systemic disorders Major trauma Massive hemorrhage Crush syndrome Spetic shock Transfusion reactions Pregnancy: postpartum hemorrhage Postoperative, particularly cardiac, aortic, and biliary surgery Major blood vessel disease Renal artery thrombosis, embolism, or stenosis Bilateral renal vein thrombosis Diseases of glomeruli and small blood vessels Acute poststreptococcal glomerulonephritis Systemic lupus erythematosus Polyarteritis nodosa Schönlein-Henoch purpura Subacute bacterial endocarditis Serum sickness Goodpasture’s syndrome Malignant hypertension Hemolytic-uremic syndrome Drug-related vasculitis Pregnancy: abruptio placentae; abortion with and without Gram-negative sepsis; Rapidly progressive glomerulonephritis, unknown etiology

  6. Specific Etiologies of Acute Renal Failure /2 II. Nephrotoxins Exogenous Heavy metals: mercury, arsenic, lead, bismuth, uranium, cadmium Carbon tetrachloride Other organic solvents X-ray contrast media Pesticides Fungicides Antibiotics: aminoglycosides, penicillins, tetracyclines, amphotericin Other drugs and chemical agents: diphenylhydantoin, phenylbtazone Endogenous Calcium (hypercalcemia) Uric acid (hyperuricemia and hyperuricosuria) Myoglobin (rhabdomyolysis) Hemoglobin (hemolysis)

  7. Course of parenchymal ARF Initiation of ARF (hours-days) Maintenance of ARF (days-weeks) Recovery (weeks-months) hemo-dynamic event tubular alterations partial toxic effect vascular alterations total glomerular capillary permeability changes in resistances backleakage of filtrate tubular obstruction

  8. Initiation of ARF (experiments and observations) 1. Hemodynamic events - transitorical renal arterial occlusion  ARF - intrarenal arterial infusion of vasoconsrictors  ARF - inhibitors of prostaglandin synthesis  incidence and severity of ARF  - in ARF: renin-angiotensin  Conclusion: During the initiation af ARF the RBF generally is decreased, later on RBF increased or normalized, but GFR still remains low. 2. Toxic effects: (experiments and life) - antibiotics (aminoglycosides, cephalosporins, colistin) - iodine-containing x-ray contrast - heavy metals (lead, arsenic, cadmium, mercury, uranium, bismuth) - organic solvent (carbon tetrachloride) - ethylene glycol (antifreeze) - anesthesics (methoxyflurane, enflurane) - cyclosporin

  9. Afferent Arteriolar Constriction A., Afferent Arteriole Efferent Arteriole RBF GFR Efferent Arteriolar Dilatation B., RBF GFR C., Diminished Glomerular Permeability RBF GFR

  10. Changes in Endothelial Fenestration of Glomerular Capillary during ARF Induced by Ischemia

  11. Changes in Podocytes’ Foot Processes of Glomerular Capillary during ARF Induced by Ischemia

  12. Possible Role of Renin Angiotensin System in the Development of ARF Ischaemia Tubular lesion Decrease of GFR Afferens arteriolar resistance Na+ concentration in distal tube and at macula densa TGF Angiotensin II Renin secretion in juxtaglomerular cells glomerular permeability

  13. 20 Endothelin Concentration (pg /ml) 10 0 Acute Renal Failure Recovery Figure: Plasma endothelin concentration during Acute Renal Failure and Recovery. The hatched area represents the normal range. Open circles denote patients who survived, and triangles patients who died

  14. Acute Renal Failure induced by uranyl nitrate (micropuncture studies at 48h) Pre-UN Post-UN Renal blood flow, ml/min Urine flow, ml/min GFR, ml/min BUN, mg% Nephron GFR, ml/min Intra-tubular pressure, mmHg Transit time, sec 174 0.12 35 13 89 16 24 204 0.02* 0.20* 120* 57* 16 24 * p < 0.001 or less.

  15. Proximal tubular pressure before renal arterial obstruction 1-3 hrs after release of obstruction % of tubules 22-26 hrs after release of obstruction 1 week after release of obstruction Proximal tubular pressure mmHg

  16. Acute Renal Failure induced by uranyl nitrate (micropuncture studies at 48h) Control n=14 UN n=17 120 100 80 (3H) inulin recovery % 60 40 20 0 Figure: Comparison of the urinary recovery of 3H-inulin injected into the proximal tubule of control and uranyl nitrate-treated dogs

  17. Nephrons disected from a human kidney during ARF

  18. Tubular obstruction Normal Afferent Arteriole Efferent Arteriole GFR H2O and Electrolytes H2O and Electrolytes Acute Renal Failure Decreased Glomerular Filtration Pressure Increased Intratubular Pressure GFR Obstruction

  19. Backleakage of Filtrate Normal Afferent Arteriole Efferent Arteriole GFR H2O and Electrolytes Inulin H2O and Electrolytes Acute Renal Failure Afferent Arteriole Efferent Arteriole SNGFR Inulin Inulin Inulin H2O and Electrolytes H2O and Electrolytes GFR

  20. Interactions of nephrotoxins or ischemia with tubular cell integrity and function. nephrotoxins ischemia Protective mechanism against lipid peroxidation Protein synthesis Membrane integrity Cytoplasmic embranes Mithocondrial inner membrane Permeability Energy production Transport Intracellular ATP , Na+ , K+ , H+ , Ca++ Free radicals , proteolysis Swelling of cells Necrosis

  21. Comparison of balance of oxygen delivery and oxygen consumption in several organs O2 consump-tion O2 delivery Blood flow rate O2 consumption/ O2 delivery % Region or organ ml/min/100g Hepato-portal Kidney Outer medulla Brain Skin Skeletal muscle Heart 11.6 84.0 7.6 10.8 2.6 0.5 16.8 58 420 190 54 13 2.7 84 2.2 6.8 6.0 3.7 0.38 0.18 11.0 18 8 79 34 15 34 65

  22. The hypothetical role of the medullary thick ascending limb of Henle’s loop (mTAL) in the pathophysiology of ischemic ARF Ischemia toxin RBF  GFR   tubular heterogeneity mTAL ischemia if SNGFR0 if SNGFR=0 transport  continue high O2 demand mTAL structure protected (PG, diuretics) mTAL damage backleak obstruction tubuloglomerular feedback 

  23. Injury to the mTAL in experimental renal ischemia 1, Controlled hemorrhagic hypotension (Bp:30-40 mmHg) produces focal mTAL damage associated decreased urinary concentrating ability before renal failure can be demostrated. 2, Recent observations show a selective decreasein the Na-K-ATPase in the outer medulla as compared to the cortex during ischemic injury. 3, mTAL injury associated with compldete arterial occlusion is much less advanced than that of hypoxia imposed during isolated perfusion.

  24. AVE Oliguric Nonoliguric 1960’s: ~ 98-100% 1990’s: ~30-80% ~ 2-0 % ~ 20-70 % Lab and Clin Complications in Oliguric and Nonoliguric ARF Oliguric (n=38) Nonoliguric (n=54) Maximum BUN 41±2 (114±5 mg/dl) 34±2 (95 ±5mg/dl) (mmol/l) Max. creatinine 796 ±44 (9 ±0.5 mg/dl) 530±26 (6 ±0.3 mg/dl) (µmol/l) Hospitalization (days) 31±3 22 ±2 Required dialysis 84% 28% Complications Gastroinestinal hemorrhage 39% 19% Infection 42% 20% Metabolic acidosis 45% 20%

  25. 100 Oliguric Nonoliguric 80 60 % ARF MORTALITY 40 20 0 Hou et al (n= 129) Frankel et al (n= 64) Rasmussen et al (n= 143) Mortality rates of oliguric and nonoliguric acute renal failure.

  26. Possible explanations for nonoliguric ARF 1, In some healthy nephronns there are still filtration but there is almost no reabsorption. 2, Decreased medullary osmotic concentration decreased reabsorption of H2O

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