RENAL FAILURE

The loss of kidney function Sudden interruption of kidney function to regulate fluid and electrolyte balance and remove toxic products from the body

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Diuretics
Are used to lower blood volume because of hypertension, congestive heart failure, or edema Increase volume of urine by increasing proportion of glomerular filtrate that is excreted Loop diuretics are most powerful; inhibit AT salt in thick ascending limb of LH Thiazide diuretics inhibit NaCl reabsorption in 1st part of DCT Carbonic anhydrase inhibitors prevent H20 reabsorption in PCT when HC0s- is reabsorbed Osmotic diuretics increase osmotic pressure of filtrate

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Diuretics and Their Mechanisms of Action

1. Osmotic Diuretics Decrease Water Reabsorption by Increasing Osmotic Pressure of Tubular Fluid 2. Loop Diuretics Decrease Active Sodium-ChloridePotassium Reabsorption in the Thick Ascending Loop of Henle 3. Thiazide Diuretics Inhibit Sodium- Chloride Reabsorption in the Early Distal Tubule 4. Carbonic Anhydrase Inhibitors Block SodiumBicarbonate Reabsorption in the Proximal Tubules 5. Competitive Inhibitors of Aldosterone Decrease Sodium Reabsorption from and Potassium Secretion into the Cortical Collecting Tubule

CLINICAL FINDINGS
OLIGURIC PHASE DIURETIC PHASE

CONVALESCENT PHASE

Hypernatremia Hypocalcemia Hyperkalemia

Hyponatremia Hypokalemia Hypovolemia

Normal Urine Volume

Increase in LOC
BUN stable and normal May develop CRF

Hyperphosphatemia
Hypermagnesemia Metabolic acidosis
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Acute Renal Failure

Prerenal Intrarenal Postrenal

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Phases of Acute Renal Failure

1. Oliguric phase 2. Diuretic phase 3. Recovery or convalescence

Four phases of acute renal failure (Brunner and Suddarth) 1. Initiation phase 2. Oliguric phase 3. Diuretic phase 4. Convalescence or recovery phase
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PRERENAL CAUSES

INTRARENAL CAUSES
Acute tubular necrosis (ATN)

POSTRENAL CAUSES
Calculi Tumors Blood clots BPH Strictures

Hypotension Cardiogenic shock

Acute vasoconstriction

Diabetes mellitus
Malignant hypertension
Acute glomerulonephritis

Hemorrhage Burns

Tumors
Blood transfusion reactions

Septicemia
CHF

Trauma
Anatomic malformation

Nephrotoxins

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NURSING CARE
Monitor fluid and electrolyte balance.

Monitor alteration in fluid volume.

Promote optimal nutritional status

Prevent complications from impaired mobility

Prevent fever and infection

Support client/S.O. & reduce/relieve anxiety
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Diagnostics
a. Increased BUN and serum creatinine level. b. Decreased urinary creatinine clearance. c. Elevated blood sugar and triglycerides. d. Increased scrum potassium. e. Anemia (decreased hemoglobin and hematocrit).

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Acute renal failure -PATHOPHYSIOLOGY

Prerenal CAUSE: Factors interfering with perfusion and resulting in diminished blood flow and glomerular filtrate, ischemia, and oliguria; include CHF, cardiogenic shock, acute vasoconstriction, hemorrhage, burns, septicemia, hypotension, anaphylaxis

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CLINICAL FINDINGS STAGE 1

Diminished Renal Reserve

STAGE 2
Renal Insufficiency

STAGE 3
End Stage

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Hemorrhage Shock Burns Hypovolemia Renal vascular obstruction -(A/V)thrombosis

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Renal insufficiency
a. GFR is 25 percent of normal. b. BUN and serum creatinine increased (azotemia). c. Fatigue and weakness, mild anemia.

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Chronic Renal Failure

Dermatologic CNS
dry skin, pruritus, uremic frost seizures, altered LOC, anorexia, fatigue

CVS
Pulmo Hema Musculoskeletal
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Acute MI, edema, hypertension, pericarditis

Uremic lungs Anemia

loss of strength, foot drop, osteodystrophy
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Chronic Renal Failure

PATHOPHYSIOLOGY STAGE 1= reduced renal reserve, 40-75% loss of nephron function STAGE 2= renal insufficiency, 75-90% loss of nephron function STAGE 3= end-stage renal disease, more than 90% loss. DIALYSIS IS THE TREATMENT!

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Renal/Intrarenal(kidney tissue pathology)

Acute tubular necrosis Nephrotoxins Aminoglycosides or NSAIDs Heavy metals -(carbon tetrachloride, arsenic,
lead, mercury

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Heart Failure

Vasodilatation

Hypovolemia

Systemic Hypotension Atherosclerois Renal Ischemia Nephrosclerosis

Renal artery stenosis

Inadequate filtration

Prerenal Disease Prerenal disease

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CLINICAL FINDINGS
Nausea and vomiting Uremic frost

Decreased urinary output

Azotemia Hypertension (later) Convulsions Pericardial friction rub
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Dyspnea
Hypotension (early) Lethargy Memory impairment CHF
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Loss of Neprhons

Glomerular hypertrophy and inc. SNGFR

Glomerulosclerosis

Accumulation of solute

Tubular hyperthrophy

High intraglomerular Pressure and inc. filtration of macromolecules Inc. excretion of Solute per nephron

Systemic Hormonal Changes in blood

Tubular cell damage & interstitial fibrosis

Extrarenal organ Damage; uremic Syndrome;toxic Effects on renal cells

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Maintenance of internal Environment up to limits of Nephron adaptation And hyperthrophy

Pathophysiology of CRF

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Chronic Renal Failure

Predisposing factors: DM= worldwide leading cause Recurrent infections Exacerbations of nephritis urinary tract obstruction hypertension

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 It occurs in stages, is irreversible, and results in uremia or end-stage renal disease CRF affects all of the major body systems and requires dialysis or kidney transplant to maintain life

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 The result is azotemia to UREMIA

The nephrons left intact are subjected to an increased work load, resulting in hypertrophy and inability to concentrate urine.

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Chronic Renal Failure

CRF is a progressive, irreversible reduction in renal function such that the kidneys are no longer able to maintain the body environment. Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction. The GFR gradually decreases as the nephrons are destroyed.
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Prerenal(renal ischemia)
Serious cardiovascular disorders Peripheral vasodilation Severe vasoconstriction

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Kidney function
The Nephron produces urine to eliminate waste Impaired urine production and azotemia Secretes Erythropoietin to ANEMIA increase RBC Metabolism of Vitamin D Calcium and Phosphate imbalances

Produces bicarbonate and Metabolic ACIDOSIS secretes acids Excretes excess POTASSIUM
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HYPERKALEMIA

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