Gastrointestinal Problems in Acute Kidney Injury

Objectives

This chapter will:

1.
Present an overview of the epidemiology, pathogenesis, and clinical features of common gastrointestinal problems associated with acute renal failure.
2.
Describe the management of common gastrointestinal problems associated with acute renal failure.

The second half of the 20th century saw remarkable changes in the clinical presentation of patients suffering from acute renal failure (ARF). These changes relate to the emergence of new nephrotoxic agents, the change in pattern of ARF-inducing diseases, and improvement of medical care through use of more effective drugs and the earlier application of efficient renal replacement therapies. Because patients with untreated terminal ARF are encountered rarely, some of the advanced gastrointestinal (GI) complications of uremia, such as stomatitis and colitis, for example, are seen less frequently than in years past. Nevertheless, certain other GI complications, such as bleeding, still warrant close attention. Furthermore, uremia-induced GI symptoms such as anorexia, dysgeusia, nausea, and vomiting continue to plague patients and often herald the need for prompt renal replacement therapy.

Pathogenesis of Uremic Lesions in the Gastrointestinal Tract

The entire GI tract may be involved in advanced uremia, with the stomach and the small and large intestines affected most commonly. Jaffe and Laing found the earliest pathologic changes in the GI tract of uremic patients to be in the form of capillary hyperemia, dilatation of submucosal veins, edema, hemorrhage, and subsequent bacterial invasion of the devitalized areas, accompanied by fibrinous exudates and necrosis.

Urea retention can impair gastric defense against autolysis. Edward and Skoryna demonstrated that an increase in gastric juice urea level may lead to dissolution of gastric mucus. In addition, by investigating ionic fluxes across the stomach of experimental animals, Davenport found that intraluminal urea in high concentrations could raise gastric permeability. A consequence of this gastric hyperpermeability is an augmented back-diffusion of hydrogen ions from the gastric lumen to the mucosa. Fisher et al. observed that gastrin could cause pyloric incompetence by antagonizing the effects of cholecystokinin and secretin on the pyloric sphincter. Gastrin is catabolized by the normal kidneys. With ARF, gastrin catabolism is impaired and plasma gastrin level commonly rises.

Wesdorp et al. observed a nearly sixfold increase in the mean plasma gastrin level in patients with ARF as compared with control subjects, with levels in approximately 20% of the patients reaching levels in the Zollinger-Ellison range. Although an elevated plasma gastrin level may foster GI bleeding and gastritis, intragastric pH is not lower in patients with renal failure. Indeed, a low basal acid output with a high basal intragastric pH, but with a significant peak acid output, has been found in patients with ARF. Moreover, pentagastrin-stimulated gastric acid secretion is normal in patients with ARF. The high basal intragastric pH may reflect the neutralizing effect of a high gastric ammonia concentration. Lieber and Lefevre detected higher gastric ammonia values and lower acid levels in uremic patients as compared with normal control subjects. Gastric ammonia levels are higher as a result of the splitting of the available higher-than-normal amounts of urea by urease-rich bacteria in the stomach. Impairment of cell renewal and cell division in ARF may reduce the competence of the mucosal barrier, contributing to the initiation and persistence of a uremic lesion by impairing epithelial wound healing.

Gastrointestinal Problems Commonly Associated With Acute Renal Failure

Dysgeusia, Anorexia, Dyspepsia, Hiccups, Nausea, and Vomiting

In uremic patients, dysgeusia commonly manifests as a metallic or a foul taste in the mouth. In addition, anorexia, dyspepsia, hiccups, nausea, and vomiting are frequent components of the uremic syndrome. Persistent vomiting may bring about dehydration (with associated dryness of the tongue and of the mouth), electrolyte disturbances, and wasting. With regard to therapy for nausea and vomiting, apart from dialysis, symptomatic improvement can be obtained with phenothiazines or metoclopramide, given either parenterally or rectally.

In hemodialysis patients, maintaining a blood urea level above 50 mmol/L (300 mg/dL) for periods of 7 to 90 days through the use of a urea-enriched dialysis solution can bring about vomiting. A rapid reduction of a very high blood urea level can lead to a constellation of manifestations known as the dialysis disequilibrium syndrome (DDS). Salient features of the syndrome include nausea and vomiting. DDS is believed to be the consequence of cerebral edema engendered by either the entry of water into brain cells during dialysis, secondary to the rapid decline in extracellular fluid osmolality, or by the induction of a dialysis-induced acidosis of the cerebrospinal fluid and of the brain.

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