pathophysiology of renal failure
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Pathophysiology ARF and CKDARF to CRF Overview
Precipitating FactorsPrerenal causes (~55%)Intrerenal causes (~40%)Postrenal causes (~5%)Predisposing FactorsAgeDMHeredity/GenesPrimary hypertensionCardio and peripheral vascular diseasesSLEAIDS
PhenomenonLegend:
Manifestation/s
Abrupt deterioration of renal structural integrityDirection of Pathogenesis (P)
Renal function compromisePossible Direction of P
Stages- Fluid and Electrolyte imbalances- Impaired wound healing- Increased susceptibility to infections- Acidosis- Gastrointestinal complications- Anemia- Increased incidence of pericarditis- Uremic encephalopathy- Platelet dysfunction
Major manifestations show:
Sustained renal damages or destruction
- Fluid and Electrolyte imbalances- Metabolic changes- Hematologic changes- Gastrointestinal changes- Immunologic changes- Changes in medication metabolism- Cardiovascular changes- Respiratory changes- Musculoskeletal changes- Integumentary changes- Neurologic changes- Reproductive chnges- Endocrine changes - Psychosocial changes
Multisystem involvement:End Stage renal Disease
Total GFR decreased
Serious inability of the kidneys to rid body of all waste productsRenal damage advances
Pathophysiology: ARF Concentration
1st Precipitating FactorsPrerenal Causes:-Volume depletion (from hemorrhage, renal losses, GI losses)-Impaired cardiac efficiency resulting from MI, heart failure, dysrhythmias, cardiogenic shock-vasodilation from sepsis
All Known Predisposing Factors
Hypovolemia
Increased osmolality of exracecellular fluidFalling O2 levels, High CO2 and H ions
Reduced arterial (e.g. carotid sinus) and cardiac baroreceptors
Excites vasomotor centerExcites osmoreceptors located @ anterior hypothalamus
Excites supraoptic nucleiIntrinsic kidney secretions causes: (Allows) vasomotor center to send vasoconstriction signals
Causes posterior pituitary to release Vasopressin ArginineProtein molecules to split causing
Almost all arterioles to constrictSmall and large veins constrictHeart stimulated to enhance pumping
Acts on the basolateral membrane of tubulesRenin release into kidney and the bloodstream
Activates the enzyme adenyl cyclase
Reacts with Angiotensinogen in liver
Causes formation of cyclic adenosine monophosphate (cyclic AMP) in cytoplasm
Angiotensin 1 released
Continues to persist in the bloodDiffuses to the laminal sideCauses mild vasoconstriction
Development of elongated vesicular structuresReacts with ACE in the lungs
Becomes Angiotensinogen 2
Fuses to the laminal membrane
Thirst mechanism activated
Inactivated by AngiotensinaseGeneral thirst sensationLaminal membrane becomes highly permeable to H2O
General constriction of arterioles
H2O moves to the inside of the cell
H2O proceeds to basolateral membrane
Causes adrenal glands to secrete AldonsteroneDecreased kidney blood flow
Drinking of H2OH2O proceeds to interstitial tissueDecreased blood flow in peritubular capillaries
Increased tubular reabsorption of sodium
Decreased fluid filters from glomeruli to tubulesRapid osmotic reabsorption of fluid from tubules
H2O conservation
Increase arterial pressure
Isovolemia or Homeostasis restoredAdequate mechanism
Possibilities
Decreased O2 delivery to proximal tubulesDecreased renal perfusionInadequate mechanism
Cycle repeats
Decreased GFR
Decreased cellular ATP
Decreased tubular flow
2nd Precipitating FactorsIntrarenal Causes:-Prolonged parenchymal ischemia from pigment nephropathy, myoglubinuria, hemoglobinuria-nephrotoxic agents- aminoglycosides, radiopaque contrast agents, heavy metals and solvents, NSAIDs, ACE inhibitors, infectious processesAll Known Predisposing Factors
1st stage
Damaged tubules
Renin-angiotensin-aldosterone reactivationInability to conserve sodium
2nd oliguric
Some cell deathMore vasoconstriction
Less fluid filteredSome tubular necrosisDecreased renal perfusion
Large numbers of excretory substances in tubules of functional nephrons
Throughout the stages: increased BUN and creatinine
3rd diuretic
Acts as osmotic diuretic pulling water with it
Rapid fluid flushing
4th recovery
Gradual improvement in metabolic waste removalToo rapid tubular fluid
Possibilities
Disruption of concentrating and diluting mechanisms
3rd Precipitating FactorsPostrenal Causes:-Urinary tract obstruction-Calculi-tumors-BPH-Strictures-Blood clotsAll Known Predisposing Factors
Obstruction @ lower urinary tract
Backing up of urine to the kidneys
Tubular damageIncreased pressure in collecting ducts and tubulesOverloading of urinary secretions
More nephrons are destroyed progressively
Pathophysiology: CRF Concentration
Precipitating FactorUntreated Acute Renal FailureAll Known Predisposing Factors
More nephrons are destroyed progressively
Decreased GFR
Inability to reabsorb electrolytesHypertrophy of remaining nephrons
Sodium wastingInadequate urine concentration
H2O wasting
Thickening or an increase in the amount of collagen in basement membrane of small vessels/tubules
Sluggish/impaired blood flow
Glomerulosclerosis
Decreased GFR
Increased vascular volumeSodium and water balance disturbedStage IDIMINISHED RENAL RESERVEGFR 50%
Edema and hypertension
More than 75% damage of nephrons
Potassium balance disturbed
Hyperkalmeia
Stage IIRenal InsufficiencyGFR 20-50%
PericarditisAccumulation of nitrogenous wastes
UremiaBUN, creatinine levels continue to rise
Skin disorders
Remaining nephrons undergo changes to compensate for those damaged nephrons
Gastrointestinal Manifestations
Filtration of more concentrated blood by the remaining nephrons
Neurologic Manifestations
Hypertrophy of nephrons
Sexual dysfunctionIntolerance and exhaustion of the remaining nephrons
Erythropoeitin production impaired
Anemia
Further damage of the nephrons
Skeletal BufferingAcid-base imbalances80-90% damage
AcidosisStage III RENAL FAILUREGFR 10-20%
OsteodystrophiesVitamin D activation impaired
Impaired kidney function and Uremia
Vitamin D activation impaired
Hyperparathyroidism
Stage IV End-Stage Renal DiseaseGFR 20% and below
Phosphate accumulation