Chronic Renal Failure
QUICK LOOK AT THE CHAPTER AHEAD
Chronic renal failure results when there is irreversible destruction of the nephrons of both kidneys and a glomerular filtration rate < 15 mL/min. In this chapter we take an in-depth look at the clinical manifestations of fluid imbalance, metabolic acidosis, and the electrolyte disturbances that occur with chronic renal failure. Treatment and nursing implications are also discussed.
 Figure 42-1 Causes and manifestations of chronic renal failure. |
CAUSES OF CHRONIC RENAL FAILUREIn chronic renal failure the glomeruli slowly sclerose, the tubules atrophy, and an interstitial fibrosis occurs. The nephrons eventually become damaged and can no longer function because they are replaced by scar tissue. The glomerular filtration rate falls to < 15 mL/min. Surprisingly, however, it takes up to 80% of nephron damage before renal function becomes clinically evident. The slow progress of this process may be caused by chronic obstruction from calculi, glomerulonephritis, or pyelonephritis. Long-term use of aminoglycoside antibiotics can result in nephrotoxicity. Diabetic nephropathy can cause chronic renal failure as well as hypertension and other vascular diseases.
Question: What is the difference between acute and chronic renal failure?
View Answer
Answer: Acute renal failure occurs secondary to an acute event and renal function returns to normal after the oliguric, diuretic, and recovery stages. Chronic renal failure occurs over time as the nephrons become permanently damaged. The kidneys do not return to normal function with chronic renal failure.
CLINICAL MANIFESTATIONS OF CHRONIC RENAL FAILUREEnd-stage renal failure is a multisystem disease. Multiple metabolic disturbances contribute to clinical manifestations with every system of the body (Table 42-1). There is no cure for renal failure other than kidney transplant provided the patient is a candidate for that procedure. Before that stage dialysis helps to keep the patient alive.
Fluid Imbalance
Unlike acute renal failure, classified by stages, chronic renal failure is progressive, beginning with a diminished renal reserve that progresses to renal insufficiency and ultimately results in end-stage renal disease. Even with a diminished renal reserve, the kidneys maintain a sufficient glomerular filtration rate to keep the serum creatinine and blood urea nitrogen levels normal. As the ability of the kidneys to concentrate urine diminishes urine output increases; this is one of the initial signs of the beginning of the disease process. Dehydration occurs if the condition goes unattended.
The progression of the disease eventually leads to a decreased number of functioning nephrons. Interestingly, the nephron is such a viable unit that dialysis is not required until almost 90% are lost. This is due to the ability of the remaining nephrons to hypertrophy and compensate for the decrease in nephron numbers. As the disease progresses the urine is no longer dilute, urine output decreases, and, if intake exceeds output, hypervolemia occurs. The ability to clear urea and other metabolic products diminishes. The progression to end-stage renal failure is reflected as a creatinine clearance of 10 mL/min compared with a normal clearance of 85 to 135 mL/min.
The ability to clear urea and other metabolic products diminishes in chronic renal failure.Table 42-1 Metabolic Disturbances of Chronic Renal Failure | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Metabolic Acidosis
The kidneys normally excrete a significant amount of acid on a daily basis. An impaired kidney, however, can neither excrete H+ nor make extra HCO3– for buffering. The amount of HCO3– that exists is used up with the circulating acid. NH4+ excretion, another method for eliminating acid, is also decreased due to the lack of available ions (see Chapter 28). Because chronic renal failure is a slowly progressing disease, the body has time to compensate for the imbalance more easily than with an acute acidotic situation.
Electrolyte Disturbances
Potassium
Oliguria is responsible for causing hyperkalemia. Potassium is primarily excreted from the body via the kidneys, and when little to no urine output exists potassium is reabsorbed. In addition, due to the acidotic state, intracellular potassium is exchanged for the excess hydrogen ion, contributing more potassium to the elevated extracellular levels. The normal therapeutic range for potassium is 3.5-5.3 mEq/L. In renal failure levels may rise as high as 7.0 or 8.0 mEq/L, contributing to life-threatening cardiac dysrhythmias and cardiac arrest.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
