Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 31: Renal Failure

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chronic and Acute Renal Failure Acute renal failure (ARF) –Sudden –Reversible Chronic renal failure (CRF) –Slow and usually insidious –Irreversible but can be slowed

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Types of ARF Prerenal –Blood supply to the kidneys Intrarenal –Damage to kidney tissue itself Postrenal –Obstructive

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Prerenal Causes of ARF Decreased kidney blood supply (perfusion) –Decreased cardiac output –Dehydration –Renal artery stenosis –Sepsis Refer to Figure 31-3.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Intrarenal Causes of ARF Directly affect kidney tissue itself –Acute tubular necrosis (ATN) –Acute glomerulonephritis (AGN) –Drug-related causes –Ischemia

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question In a patient with acute renal failure, which of the following medications is most likely the cause? A. Spironolactone (Aldactone) B. Digoxin (Lanoxin) C. Furosemide (Lasix) D. Streptomycin sulfate

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer D. Streptomycin sulfate Rationale: Streptomycin is one of the major causes of drug-induced ATN. It is an aminoglycoside antibiotic and therefore is used for more serious infections and TB. The other medications do not affect kidney necrosis. Spironolactone and furosemide are commonly used diuretics that are indicated in the hypovolemic stages of renal failure. Digoxin is a cardiac glycoside that is used to increase the strength of cardiac contraction to help decrease the preload in some types of renal failure.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Postrenal Causes of ARF This is obstructive: either in the kidney itself or in the outflow tracts Kidney obstructions –Kidney stones –Tumors Outflow tract obstructions –Ureter stones –Tumors (benign prostatic hypertrophy, prostate cancer)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pathophysiology of Prerenal ARF Decreased blood supply to the kidney Stimulation of renin-angiotensin-aldosterone system Retention of sodium and water Signs/Symptoms –Decreased urinary output (<400 mL/day) –Elevated BP Lab values –Increased urine specific gravity –Decreased urine sodium

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Treatment and Nursing Care: Early Identification High index of suspicion Increase IV fluids –Usually fluid challenge of 250 cc NSS –Look for increased urinary output and no crackles in the lungs Increased cardiac output –Watch for changes in BNP Treat any cardiac rhythm disturbances Monitor use of ACE inhibitors and NSAIDs (can make worse) Monitor BUN, creatinine, GRF

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pathophysiology of Intrarenal ARF Direct damage to kidney tissue (nephrons, cortex) from acute tubular necrosis (ATN) or ischemia (decreased blood supply) Results in tubular swelling and eventually necrosis Kidney cells block kidney blood and filtrate flow Refer to Figure 31-2.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Toxic Substances and ATN Nonoliguric Healing is more rapid Aminoglycosides Diagnostic study dyes

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nephrotoxicity (ATN) from Contrast Dye Mild Nonoliguric Reversible Increased risk in patients with: –Diabetes mellitus –Fluid volume deficit –Multiple myeloma –Increased frequency and volume of dye

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Treatment and Nursing Care High index of suspicion –High, uncontrolled glucose levels –Decreased urinary output –High BUN and creatinine Forcing IV fluids as tolerated Administration of acetylcysteine (Mucomyst)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pathophysiology of Postrenal ARF Obstruction to urinary flow Leads to increased GFR –Increased absorption of sodium and water Dilation of flow system Both kidneys must be obstructed If relieved, great increase in urinary flow Labs (same as for other types of renal failure)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Treatment and Nursing Care High index of suspicion Relieve the obstruction by mechanical or surgical methods Watch for postobstructive diuresis and resultant fluid volume deficit

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question The patient who is most likely to experience nonoliguric renal failure is one who has had a cardiac catheterization. A.True B.False

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer A. True Rationale: A large amount of dye is injected during a cardiac catheterization (coronary angiogram). This begins around 48 hours after drug administration, peaks in 3 days, and is completely excreted within a week to 10 days. Therefore, if a patient is discharged early after a catheterization, patient teaching regarding this risk is important.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins The Four Phases of ATN Onset Oliguric or nonoliguric phase Diuretic phase Recovery

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Phases of ATN: Onset Initial injury to kidney cells Important to determine the cause Important to prevent progression

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient is admitted with ATN due to use of aminoglycosides. Which of the following potassium values would be characteristic of the nonoliguric phase of ATN? A. 2.8 mEq/L B. 3.7 mEq/L C. 4.5 mEq/L D. 5.9 mEq/L

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer D. 5.9 mEq/L Rationale: A patient with nonoliguric ATN can still have a mild form of hyperkalemia, which is indicated in answer D. Answers B and D are normal potassium values. Hypokalemia, which is answer A, is not seen when the kidneys fail.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Phases of ATN: Oliguric and Nonoliguric Phases Oliguric PhaseHigher mortality rates More likely to need dialysis Fluid overload, azotemia Labs: high K+ & phosphate levels, and acidosis, low Ca+ Nonoliguric PhaseMilder form Less likely to need dialysis Fluid complications lower Labs: Monitor K+, but not as much of a problem.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Phases of ATN: Diuretic Phase Usually 1-2 weeks Urinary output gradually increases –Hypovolemia can result Nonoliguric ATN does not do this Complications –Hypovolemia –Hypokalemia

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Phases of ATN: Recovery Several months to a year Lab values drop If significant damage to kidney or basement membrane, cells will not regenerate and patient will require dialysis 45% make a complete recovery

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins How Is ARF Diagnosed? History Physical examination Lab studies

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Major Causes of ARF Diabetes mellitus Hypertension

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins How Is ARF Accelerated? Decreased kidney perfusion Introduction of nephrotoxic substances Urinary obstructions Urinary tract infections Increase in circulating lipids?

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Teaching to Prevent the Acceleration of ARF Maintain a normal BP and glucose control Drink fluids and avoid becoming dehydrated Monitor weight frequently Avoid medications that can accelerate renal failure (dyes, aminoglycoside antibiotics) Exercise Take ACE inhibitors or ARBs as directed Moderate protein ingestion with low-cholesterol diet

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Three Types of Chronic Renal Failure (CRF) Decreased renal reserveLoss of kidney function by %. Slight elevation in BUN, creatinine. Renal insufficiency60-80% of renal function is lost. Azotemia, electrolyte imbalances, anemia. Fatigue, polyuria, nocturia. End-stage renal disease (ESRD)Renal function <85%. Markedly elevated BUN, creatinine. High K+ & phosphorus, low Ca+. Changes in LOR with uremia. Dialysis needed or death will result.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management of Chronic Kidney Disease Pulmonary needs –Pulmonary edema Cardiovascular management strategies –HTN, hyperkalemia and pericarditis Acid-base management –Metabolic acidosis

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management of Chronic Kidney Disease (cont.) Neuromuscular challenges –RLS, changes in LOR Hematological alterations Skin needs Nutritional management