PATHOPHYSIOLOGY OF END STAGE RENAL FAILURE SECONDARY TO HYPERTENSIVE NEPHROSCLEROSIS

Predisposing Factors Precipitating Factors

Age (48 y/o) Lifestyle (alcoholic)
Diabetes Mellitus

Narrowing of preglomerular
arteries & arterioles

Reduction in glomerular blood

flow

Compensation for loss of renal

circulation

Destruction of Renal Papillae

Unremitting deterioration of the

kidneys

Urine may contain abnormal amounts of

Hematuria, Proteinuria, Oliguria CHON, RBCs and WBCs. Major end
products of excretion remains essentially
normal. (Stage 1 >75% GFR)

Progressive nephron
damage
PATHOPHYSIOLOGY OF END STAGE RENAL FAILURE SECONDARY TO HYPERTENSIVE NEPHROSCLEROSIS

Remaining nephrons are highly

susceptible to failing themselves as
their load becomes overwhelming.
(Stage 2 51-74 % GFR)

Surviving nephrons increase their rates of

filtration, reabsorption and secretion and
undergo hypertrophy in the process

Renal insufficiency (Stage 3 25- 50% normal

GFR)

Compensatory excretion continues

as GFR diminishes and more
nephrons progressively die. (Stage 4
12 to 24% GFR)

Plasma creatinine level increases

proportionately without regulatory
adjustment.

Sodium delivery to the nephron

increases but less is restored

Develops into Na deficits and

volume depletion
 PATHOPHYSIOLOGY OF END STAGE RENAL FAILURE SECONDARY TO HYPERTENSIVE NEPHROSCLEROSIS

Sodium retention
Edema, Hypervolemia

Lasix Kidney becomes incapable of

concentrating and diluting urine

Scar tissue and tubular atrophy are

present throughout the kidneys

End Stage Renal Failure (<12% normal GFR)

Captopril Secondary to hypertensive nephrosclerosis

Hypertension, pneumonia & Increased renin released

coupled with fluid
Pleural effusion overload

Oxidative Stress
Zosyn & Fluimicil
Anemia Failure of adequate
production of erythropoietin
PATHOPHYSIOLOGY OF END STAGE RENAL FAILURE SECONDARY TO HYPERTENSIVE NEPHROSCLEROSIS

Decreased tissue oxygenation

throughout the body

Activation of reflexes aimed at

increasing cardiac output to
improve oxygenation

Increased cardiac output

Increase resistance to the

right ventricle

Progressive right ventricle

hypertrophy

Dilated cardiomyopathy
 PATHOPHYSIOLOGY OF END STAGE RENAL FAILURE SECONDARY TO HYPERTENSIVE NEPHROSCLEROSIS

CONGESTIVE HEART
Mechanical Ventilator FAILURE

With medical intervention Without Medical Intervention

Antimicrobial Therapy, Decreased perfusion

Aerosolized medications
O2 therapy,
Fluid Replacement, Necrosis and organ failure
Dietary management,
Dialysis, renal transplant
& Multiple Organ Dysfunction
Mechanical ventilation Syndrome

Bad Prognosis
Significant improvement in
the quality of life. DEATH

Good Prognosis