Renal failure clinical presentation

The development of acute renal failure (ARF) presents a difficult challenge to the clinician. It has widely varying causes, and unlike other cases of organ failure such as neurologic or cardiovascular failure, the onset of ARF is often silent. In the ambulatory setting, patients may not notice ARF symptoms for days or weeks. Clinical and laboratory markers of its presence can be subtle and are often overlooked. Despite its often insidious presentation, ARF can be one of the most serious consequences that can occur, especially in a hospitalized patient. 

Acute allergic interstitial nephritis is the underlying cause for up to 3% of all cases of acute renal failure. Clinical manifestations of AIN typically present about 14 days after initiation of therapy and include fever, maculopapular rash, eosinophilia, pyuria, hematuria, proteinuria, and oliguria. 

Patients with either acute or chronic renal failure may present with many and varied manifestations of uremia [12]. In these patients, the application of biomarkers of effect to detect clinical disease in its earliest stages is of great importance. Table 2 contains a list of various groups of xenobiotics associated with acute or chronic renal disease. 

In clinical trials, ATI antagonists have proven to be as effective as ACE inhibitors in hypertension, congestive heart failure, and renal failure [3]. The favorable side effect profile of ATI antagonists argues for a greater use of these diugs. At present, due to still higher costs, they are indicated in patients who do not tolerate ACE inhibitor treatment. 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

The clinical presentation for IE is quite variable and often nonspecific. A fever is the most frequent and persistent symptom in patients but may be blunted with previous antibiotic use, congestive hear failure, chronic liver or renal failure, or infection caused by a less virulent organism (i.e., subacute disease).3 Other signs and symptoms that also may occur are listed in the Clinical Presentation box with some discussed further in detail below. 

Renal Effects. The patient described by Letz et al. (1984) (see Section 2.2.3.1) who lived for 64 hours after exposure to toxic levels of 1,2-dibromoethane had acute renal failure as evidenced by severe oliguria 24 hours after exposure and abnormal clinical chemistry values (blood urea nitrogen, creatinine, and serum uric acid). Severe metabolic acidosis was present despite two hemodialysis procedures. 

Complications included acute respiratory distress syndrome, renal failure, and multi-organ failure. Evidence that the clinical spectrum of human H5N1 infections is not restricted to pulmonary symptoms was provided by a reported case of possible central nervous system involvement in a Vietnamese boy who presented with diarrhea, followed by coma and death. Influenza H5N1 virus was isolated from throat, rectal, blood, and cerebrospinal fluid specimens, suggesting widely disseminated viral replication. 

Hootkins R, Fenves AZ, Stephens MK. Acute renal failure secondary to oral ciprofloxacin therapy a presentation of three cases and a review of the literature. Clinical nephrology. 1989 Aug 32(2) 75-8. 

In patients with renal failure, the occurrence of conditioned zinc deficiency may be the result of a mixture of factors, which at present are ill defined. If 1,25-dihydroxycholecalciferol plays a role in the intestinal absorption of zinc, an impairment in its formation by the diseased kidney would be expected to result in malabsorption of zinc. It seems likely that plasma and soft tissue concentrations of zinc may be "protected in some individuals with renal failure by the dissolution of bone which occurs as a result of increased parathyroid activity in response to low serum calcium. In experimental animals, calcium deficiency has been shown to cause release of zinc from bone. In some patients who are successfully treated for hyperphosphatemia and hypocalcemia, the plama zinc concentration may be expected to decline because of the deposition of zinc along with calcium in bone. Thus, in the latter group in particular, a diet low in protein and high in refined cereal products and fat would be expected to contribute to a conditioned deficiency of zinc. Such a diet would be low in zinc. The patients reported by Mansouri et al. (37), who were treated with a diet containing 20-30 g of protein daily and who had low plasma concentrations of zinc, appear to represent such a clinical instance. Presumably the patients of Halsted and Smith (38) were similarly restricted in dietary protein. In other patients with renal failure whose dietary protein was not restricted, plasma zinc concentration were not decreased. Patients on dialysis had even higher levels, particularly... 

Chronic salicylism presents clinically in a similar fashion to the acute situation, although it is often associated with a delay in diagnosis, and a higher morbidity and mortality. Chronic salicylism is more often associated with pronounced hyperventilation, dehydration, pulmonary edema, renal failure, coma, seizures, and acidosis. Chronic salicylism can occur at serum salicylate levels as low as 15mgdl. ... 

Autonomic neuropathy presents clinically as damage to the cardiovascular, genitourinary and gastrointestinal tracts. The mortality rate appears to be high (50% in 3 years) resulting from renal failure and sudden unexpected death . 

---