Pathophysiology

ARF to CRF Overview

Legend:

Direction of Pathogenesis (P)

Possible Direction of P

Predisposing Factors- Age- DM- Heredity/Genes- Primary hypertension- Cardio and peripheral

vascular diseases- SLE- AIDS

Precipitating Factors

Prerenal causes (~55%)

Intrerenal causes (~40%)

Postrenal causes (~5%)

Abrupt deterioration of renal structural integrity

Renal function compromise

Major manifestations show:

Sustained renal damages or destruction

- Fluid and Electrolyte imbalances- Impaired wound healing- Increased susceptibility to infections- Acidosis- Gastrointestinal complications- Anemia- Increased incidence of pericarditis- Uremic encephalopathy- Platelet dysfunction

Total GFR decreased

Renal damage advances

Serious inability of the kidneys to rid body of all waste products

Multisystem involvement:

- 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

End Stage renal Disease

Phenomenon

Manifestation/s

Stages

Pathophysiology: ARF Concentration

All Known Predisposing Factors

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

Hypovolemia

Reduced arterial (e.g. carotid sinus) and cardiac baroreceptors

Falling O2 levels, High CO2 and H ions

(Allows) vasomotor center to send vasoconstriction signals

1. Almost all arterioles to constrict2. Small and large veins constrict3. Heart stimulated to enhance

pumping

Excites vasomotor center

Intrinsic kidney secretions causes:

Protein molecules to split causing

Renin release into kidney and the bloodstream

Reacts with Angiotensinogen in liver

Angiotensin 1 released

Causes mild vasoconstriction

Continues to persist in the blood

Reacts with ACE in the lungs

Becomes Angiotensinogen 2

Increased osmolality of exracecellular fluid

Excites osmoreceptors located @ anterior hypothalamus

Excites supraoptic nuclei

Causes posterior pituitary to release Vasopressin Arginine

Acts on the basolateral membrane of tubules

Activates the enzyme adenyl cyclase

Causes formation of cyclic adenosine monophosphate (cyclic AMP) in cytoplasm

Diffuses to the laminal side

Development of elongated vesicular structures

Fuses to the laminal membrane Thirst mechanism

activated

Possibilities

Laminal membrane becomes highly permeable to H2O

H2O moves to the inside of the cell

H2O proceeds to basolateral membrane

H2O proceeds to interstitial tissue

General thirst sensation

Drinking of H2O

Inactivated by Angiotensinase

General constriction of arterioles

Causes adrenal glands to secrete Aldonsterone

Increased tubular reabsorption of sodium

Rapid osmotic reabsorption of fluid from tubules

Decreased kidney blood flow

Decreased blood flow in peritubular capillaries

Decreased fluid filters from glomeruli to tubules

H2O conservation

Increase arterial pressure

Adequate mechanism

Inadequate mechanism

Isovolemia or Homeostasis restored

Cycle repeats Decreased renal perfusion

Decreased GFR

Decreased cellular ATP

Decreased O2 delivery to proximal

tubules

Decreased tubular flow

Possibilities

Damaged tubules

Inability to conserve sodium

Some tubular necrosis

Some cell death

1st stage

Renin-angiotensin-aldosterone reactivation

Decreased renal perfusion

More vasoconstriction

Large numbers of excretory substances in tubules of

functional nephrons

Less fluid filtered

2nd oliguric

Acts as osmotic diuretic pulling water

with it

Rapid fluid flushing

Too rapid tubular fluid

Gradual improvement in metabolic waste removal

Disruption of concentrating and diluting mechanisms

3rd diuretic

4th recovery

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 processes

All Known Predisposing Factors

Throughout the stages: increased BUN and creatinine

Tubular damageIncreased pressure in collecting ducts and

tubules

Backing up of urine to the kidneys

Obstruction @ lower urinary tract

Overloading of urinary secretions

3rd Precipitating FactorsPostrenal Causes:-Urinary tract obstruction-Calculi-tumors-BPH-Strictures-Blood clots

All Known Predisposing Factors

More nephrons are destroyed progressively

Pathophysiology: CRF Concentration

More nephrons are destroyed progressively

Decreased GFR

Hypertrophy of remaining nephrons

Inadequate urine concentration

Inability to reabsorb electrolytes

Sodium wasting

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

Precipitating Factor

Untreated Acute Renal Failure

All Known Predisposing Factors

Stage I DIMINISHED RENAL RESERVE

GFR 50%

More than 75% damage of nephrons

Stage IIRenal InsufficiencyGFR 20-50%

BUN, creatinine levels continue to rise

Remaining nephrons undergo changes to compensate for those damaged nephrons

Filtration of more concentrated blood by the remaining nephrons

Hypertrophy of nephrons

Intolerance and exhaustion of the remaining nephrons

Further damage of the nephrons

80-90% damage

Stage III RENAL FAILUREGFR 10-20%

Impaired kidney function and

Uremia

Stage IV End-Stage Renal Disease

GFR 20% and below

Sodium and water balance disturbed

Potassium balance disturbed

Uremia

Erythropoeitin production impaired

Acid-base imbalances

Vitamin D activation impaired

Phosphate accumulation

Increased vascular volume

Please note that due to the complexity of the disease process, I have deemed necessary not to include the management both medical and nursing related in this diagram. Furthermore, only important manifestations were included also. Readers are encouraged to continue reading instead for it is indicated below.

Edema and hypertension

Hyperkalmeia

Anemia

Skeletal Buffering

Acidosis

Vitamin D activation impaired

Hyperparathyroidism

Osteodystrophies

Accumulation of nitrogenous wastes

Pericarditis

Sexual dysfunction

Skin disorders

Gastrointestinal Manifestations

Neurologic Manifestations