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Kelly, Maryann

AJN The American Journal of Nursing: April 1996 - Volume 96 - Issue 4 - p 21

Author Maryann Kelly replies: Due to the space limitations of a "Clinical Snapshot," full details of nursing care or drug precautions can't be included. The purpose of these features is to provide the reader with a "glimpse" of the subject. Also, it must be remembered that the article addressed chronic renal failure, not ESRD.

In reply to the criticism, "rarely does an obstruction lead to chronic renal failure": As mentioned, there are various stages of CRF, from mild renal insufficiency (loss of 25% to 30% of renal function) to advanced renal failure (loss of 80% to 90%). End-stage renal failure denotes that stage of CRF that requires dialysis or transplantation (usually less than 5% of normal renal function).

It's well known that complete ureteral obstruction eventually destroys renal function. The postulated mechanisms are elevated ureteral pressure and decreased renal blood flow, which cause cellular atrophy and necrosis. The pathophysiologic effects of short-term complete obstructive uropathy or chronic partial obstructive uropathy can be summarized simply: All renal functions except urinary dilution are progressively impaired; the longer or more severe the obstruction, the more renal damage will result.

How long can the human kidney be completely obstructed before it sustains enough damage to prevent any recovery of function after release? Return of function may well depend upon many factors other than period of obstruction, such as absence of infection. Presumably, incomplete ureteral obstruction will destroy renal function slowly, but it certainly can progress to complete functional destruction. The loss of renal function due to partial obstruction is seen clinically with silent prostatism or ureteropelvic junction obstruction.

It is generally believed that the post-obstructed kidney exhibits a reduction in glomerular filtration, blood flow, concentrating ability, hydrogen ion clearance, and phosphate excretion. Sodium reabsorption is mildly impaired, while urinary dilution isn't affected.

Tumors, including benign or malignant and primary or metastatic types, mass lesions such as cysts or lymphoceles, aneurysms, vascular anomalies, fluid such as blood or pus, and infectious as well as inflammatory processes may affect the ureter. When the obstruction is bilateral, is slow in developing, and has been present a long time, severe renal failure with its accompanying complications may be the presenting problem. (Campbell's Urology, 4th ed., W. B. Saunders Co., pp. 377-413, 415-447; Clinical Geriatrics, 3rd ed., J. B. Lippincott Co. (London), pp. 215-229)

As to Ms. Olson's point "Demerol is contraindicated for pain," again, space limitations precluded discussion of this particular drug. Chronic renal failure is a relative contraindication for Demerol. Demerol must be used in the same judicious manner as one would use when giving vancomycin to a patient with CRF. One nephrologist that I contacted said, "I see no problem with giving Demerol to a patient in CRF, but one must know the drug and the patient before giving any drug." I contacted several dialysis units in my area, and they don't consider Demerol contraindicated.

The Physician's Desk Reference states under "Precautions": "Meperidine should be given with caution and the initial dose should be reduced in certain patients such as the elderly or debilitated, and those with severe impairment of hepatic or renal function, hypothyroidism, Addison's disease, and prostatic hypertrophy or urethral stricture." Elsewhere, it has been suggested that "normeperidine toxicity may be prevented by avoiding prolonged administration of meperidine, especially to patients with impaired renal function" (Anesth.Analg. 65:536-538, 1986).

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