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Chapter 13 Renal Failure

Chapter 13 Renal Failure. §1 Concept & Introduction. Kidney structure: Nephron (Glomerulus & Tubules) ,/ Renal interstitium ,/ Kidney blood vessels, / Urinary tract outside kidney( Ureters & bladder )

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Chapter 13 Renal Failure

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  1. Chapter 13 Renal Failure

  2. §1 Concept & Introduction • Kidney structure: Nephron (Glomerulus & Tubules) ,/ Renal interstitium ,/ Kidney blood vessels, / Urinary tract outside kidney( Ureters & bladder ) • Many pysiologecal function:⑴Excretory function ⑵Regulatory function ⑶Endocrine and metabolic function

  3. Reabsorption and secretion In tubules Filtration function in glomerulus Excretory function & Endocrine function • Excretory function GFR (125ml/min) 99% Urine (1.5~2L / d ) Removal of waste products,drug and toxic substances Maintenance of water, electrolyte and acid-base balance Maintenance of volume and composition in urine RF Azotemia,Hyperkalemia,Metabolic acidosis, Water intoxication,Oliguria,Anuria/Non-oliguria, Alteration of composition in urine

  4. RF RF Endocrine functions: • Renin (R) ↑ Renal hypertension • Prostaglandins(PG)↓ Renal hypertension • Kallikrein & Kinin↓ Renal hypertension • Erythropoietin(EOP) ↓Renal anemia • 1,25-(OH)2-D3 ↓Renal osteodystrophy hyperphosphatemia hypocalcemia • Intrarenal R-A system • Intrarenal K-K-P system • Intrarenal ET-NO/NOS system Acute renal failure, Chronic renal failure, Uremia RF RF RF

  5. §2 Acute Renal Failure (ARF) • Concept ARF is a complex pathophysiologic process and is an important clinical syndrome. It is characterizedby sudden decline in renal excretory function over a period and usually associated with oliguria, anuria / non-oliguria, Alteration of composition in urine, azotemia, hyperkalemia, metabolic acidosis and water intoxication. • Causes (1) Prerenal causes(renal hypoperfusion) Prerenal ARF Blood supply to nephron↓----CO↓,/ Bp ↓,/ BV ↓,/ Constriction of kidney blood vessels.

  6. Alterations of volume and composition in urine: Oliguria (<400ml/d) or Anuria (<100ml/d) Urinary Na+ ↓(<20mmol/L ) Urine specific gravity ↑(>1.020) Urine osmolality ↑(>400mosm/L) Ucr / Pcr ↑(>40:1) RFI < 1 FENa <1 Urine sedimentary assay: (-) Prerenal causes Renal perfusion ↓ GFR↓ ADH↑,ADS↑ RFI=Urinary Na+∕ Ucr/Pcr FENa=Urinary Na+/blood Na+/ Ucr/Pcr

  7. (2) Intrarenal causes (intrinsic renal injury)  Intrarenal ARF Injury of renal tissue itself (glomerulus,/ tubules,/ blood vessels) 1) Diseases of glomerulus--- Acute poststreptococcal glomerulonephritis,/ Vasculitis 2) Acute tubular necrosis (ATN)---Severe renal ischemia ,/ Renal poisoning (Heavy metals,/ ethylene glycol ,/ Insecticide ,/ Poisonous mushrooms, / Carbon tetrachloride ) A number of chemical agents can selectively and critically destroy renal tubular cells. 3)Renal vessel injury--- Embolism of renal artery,/ DIC 4)Renal interstitial injury---Acute interstitial nephritis,/ Bilatenal pyelonephritis

  8. Oliguria,Anuria or Non-oliguria ( ≈1000ml/d) Urinary Na+↑(>40mmol/L ) Urine specific gravity ↓(<1.015) Urine osmollarit↓ (<350mOsm/L) Ucr / Pcr ↓(<20:1) RFI >1 FENa >2 Urine sedimentary assay: Proteinuria, Cylindruria,Blood urine. Alteration of volume and composition in urine: Severe renal ischemia Renal poisoinig Renal perfusion ↓ GFR ↓ ATN (3)Postrenal causesPostrenal ARF Obstructive disorders in urinary tract--- large stone,/ Blood clots,/ Scarring of injury or surgery.

  9. 3.Pathogenesis of ARF 1.Renal hemodynamic alterations (Vasomotor theory) → GFR↓ (1)Decrease of renal perfusion pressure arterial blood pressure↓→ Renal blood pressure↓ (2)Renal vasoconstriction Renin-angiotensin system ↑ATⅡ↑ Sympathetic adrenergic system↑ Catecholamine↑, Prostacyclin↓,Endothelin(ET)↑,Nitric oxide(NO)↓, 3)Renal vascular endothelial swelling Hemodynamic factors play an important role predominatly during the initiation of the acute renal insult.

  10. (4)Ischemia-reperfusion injury of Kidney . Calcium overload(Calcium paradox) / Active xanthine oxydase (XO) Oxygen flee radicalsobstruct renal capillary and cause tubular necrosis 2.Renal glomerular injury Acute glomerulonephritis,lupus nephritis→glomerular membrane damage→ filtration area↓→GFR↓ 3. Renal tubular injury (1)Passive backflow (Back-Leakage theory) (2)Tubule obstruction (Tubule obstruction theory) 4.Renal cell injury(endothelial、mesangial cells etc.)

  11. Renal ischemia,renal poisons Injury of renal tubular cells Loss of Tubule Integrity Cellular Debris Back-leakage of crude urine Tubular Obstruction ↓ Effective Filtration pressure ↓Glomerular filtration rate Oliguria

  12. 4.Alterations of metabolism and function • Oliguric Acute Renal Failure 1.Oliguric phase (1) Urinous alterrations :Oliguria / Anuria, Alteration of composition in urine. as following (2) Azotemia ---an abnormally high level of nitrogenous wastes (blood urea nitrogen, uric acid, serum creatinine)  Autotoxication Syndrome (3) Water intoxicationDiluted hyponatremiaCerebral edema, Pulmonary edema, Cardiac insufficiency (4) Hyperkalemia Myocardial poisoning (5) Metabolic acidosis Hyperkalemia, Disfunction of CNS

  13. 2.Diuretic phase Urine volume>400ml/d, → >3000ml/d. In the early pase, BUN, serum creatinine, potassium, and phosphate may remain elevated or continue to rise even though urine output is increased. In the late phase, dehydration,hypokalemia,hypernatremia are easy to occur. 3. Recovery phase

  14. Nonoliguric ARFis another type of ARF,in which renal pathological changes And clinical presentations are relatively slight, so the disease is shorter, and Prognosis is better. Its main characters include ① urine output not decrease (400～1000ml/d); ② special gravity of urine is low and fixed, and urinous sodium Content is low; ③ existence of azotemia. The mechanism for this type of ARF is Not understood currently.

  15. §3 Chronic Renal Failure(CRF) • Concept CRF a complex pathophysiologicprocess and is an important clinical syndrome It is characterized by progressive and irreversible destruction of renal tissue.The Consequences of renal destruction express in progressive deterioration of the filtration,reabsorptive functions and endocrine functions of the kidney, damage usually proceeds slowly, terminating in death when a sufficient number of nephrons have been destroyed. The end stage of CRF is uremia.

  16. 2. Causes Any disorder that permanently destroys nephrons may result in CRF ( by glomeruli, tubules, renal interstitium, blood vessels ,lower urinary tract,) Exemplum : 1) Chronic glomerulonephritis---by destruction of glomeruli. 2) Chronic pyelonephritis---by fibrosis of renal pelvis and medulla. 3) Hypertension nephropathy---by narrowing of renal arteries. 4) Renal calculi, urethral or ureteral stricture---by damage to the nephrons caused by fluid back-pressure secondary to obstruction.

  17. 3.Clinical Course of CRF • Stage of decreased renal reserve(Silent stage) Ccr>30%, BUN and serum creatinine(Cr) = nomal, Renal reserve ↓. [ Clearancecreatinine=Ucr x V / Pcr ≈ GFR ] (2)Stage of renal insufficiency Ccr=25~30%, BUN and Cr ↑, Polyuria, Nocturia, Mild anemia and acidosis. (3)Stage of renal failure Ccr=20~25%,Marked anemia, severe acidosis, hypocalcemia, hyperphosphatemia, BUN and Cr↑↑. (4)Stage of uremia Ccr<20%,A series of uremic symptoms, The uremic syndrome affects every system in the body. .

  18. 4.Pathogenesis of CRF • Intact nephron hypothesois Intact nephron hypertrophy (filtration↑reabsorption↑) Destroyed nephron (filtration↓reabsorption↓) (2) Trade-off hypothesis “Trade off” refers a process that organism develops a new lesion by Correcting an old damage: AS the nephrons are progressively destroyed, increased blood concentration of some solutes stimulates secretion of some relatedregulatory factors (such as hormones) in order to maintain the excretion function. At the same time, however, high blood levels of the regulatory factors will result in further metabolic disorder. It is termed ”trade-off”.

  19. GFR↓→filtration of phosphate↓→plasma phosphate↑and plasma calcium↓→PTH↑→plasma phosphate(N)… GFR↓↓→Plasma phosphate↑↑→PTH↑↑→breakdown of bone →hyperphosphatemia and renal osteodystrophy

  20. (3)Glomerular hyperfiltration hypothesis In the single nephron compensatory intraglomerular hyperfusion and hyperfiltration, together with intraglomerular hypertension result in progressive glomerular sclerosis and eventual glomerular death Several hormones, growth factor, biologically active lipids cytokines (ATⅡ,TGF-β,IL-1, TNF ) influence mesangial and interstitial cell proliferation and extracellular matrix deposition → nephrons↓→ vicious circle → CRF (4)Lesion of tubular and interstitial cells

  21. 5.Alterations of metabolism add function (1)Disturbance of water, electrolyte and acid-base ①Disorders of water balance Nocturia (the urine volume in night time is about 2~3 times in day time, or more than 750ml ) at GFR<40ml/min Polyuria (>2000ml/d) at GFR<30ml/min Oliguria (<400ml/d) at GFR=5~10ml/min Hyposthenuria(<1.020), Isostheuria(1.010, 285mOsm/L) Proteinuria ,Cylindruria . .

  22. ②Disorders of electrolyte metabolism • Disorders of sodium metabolism Hyponatremia ( when polyuria) ↓ hypernatremia (When oliguria) • Disorders of potassium metablism Serum potassium concentration is usually maintained normal range until GFR<25%. Polyuria in early CRF→hypokalemia. Oliguria in end-stage CRF→hyperkalimia.

  23. Disordrs of calcium-phosphate balance Hyperphosphatemia GFR↓→filtration of phosphate↓→plasma phosphate↑and plasma calcium↓→PTH↑→plasma phosphate(N)… GFR↓↓→Plasma phosphate↑↑→PTH↑↑→breakdown of bone→hyperphosphatemia. Hypocalcemia hyperphosphatemia / vitaminD3 metabolism dysfunction/ PTH↑calcitonin secretion ↑ / some toxic substances damage GI to reduce Ca2+absorption. • Metabolic acidosis Impaired ability of the kidney to excrete, H+/ NH4+ excretion is decreased GFR↓→retention of phosphate,sulfate and other organic anions

  24. (2) Azotemia Non-protein nitrogens( NPN)>28.6mmol/L or >40mg/dl Blood urea nitrogen( BUN)>3.75~7.14mmol/L or >10~20mg/dl Plasma creatinine (Scr)>0.9~1.8mg/dl [ Creance clearance=Ucr x V(ml/min) / Pcr ≈GFR .] Blood uric acid >3~5mg/dl (3)Renal hypertension Sodium-dependent hypertension Renin-dependent hypertension PGE2↓,PGI2↓and KK-K↓→hypotension

  25. (4)Renal osteodystrophy which includes renal rickets (for children),adult osteomalacia, osteitis fibrosa,osteoporosis

  26. Chronic renal Failure GFR↓ 1,25(OH)2Vit.D3↓Elimination of phosphate ↓ Acidosis Plasma phosphate↑ Deposition of Gastrointestinal Calcium in bone↓ absorption of calcium↓ Hypocalcemia Secondary hyperparathyroidism Renal osteodystrophy

  27. (5) Renal anemia Mechanism Reducing erythropoiten / Cumulating of toxic substances in body / Bleeding / Toxic substances destroy RBCs / Reducing absorption or utilization of iron and protein (6)Tendency to hemorrhage Mechanism: by inhibiting role of the cumulating renal poisons (such as urea, Carbamidine,etc.) on function of platelet

  28. §4 Uremia 1.Concept of uremia Uremia is the most severe stage of acute or chronic Renal failure .Besides disorders of water and electrolyte metabolism and acid-base imbalance, and renal endocrine function, the patients with uremia will manifest a series of autotoxication syndroms caused by accumulation of endogenous poisons. 2.Clinical manifestation of uremia (1)Nenrological signs (2)Cardiovascular signs (3)Respiratory signs (4)Gastrointestinal signs (5)Endocrine signs (6)Signs of skin (7)Immunity signs (8)Disorders of metabolism

  29. 3.Pathogenesis of uremia • Uremic Toxins ①Urea ②Guanidine compound ③Amines and phenols ④Middle molecules(mol.wt.500~5000D) (2) Parathyroid hormone (PTH) (3)Aluminum

  30. Pathophysiological basis of prevention and treatment For the treated of ARF are as following: 1.To maintain fluid and electrolyte, acid-base, and solute homeostasis, such as treating hyperkalemia and correcting metabolic acidosis 2.To control the level of blood nonprotein nitrogen. 3.To prevent subsequent infection. 4.To promote healing and renal recovery. 5.To permit other support measures, such as nutrition to proceed without limitation. 6.Renal replacement therapy may be provided by peritoneal dialysis or intermittent hemodialysis. For the treated of CRF and uremia are as following 1.To treat the primary renal disease. 2.To treat reversible aggravating factor. 3.To prevent or slow the progression of real disease. 4.To prevent and treat end stage renal failure. 5.Other treatment.

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