- What underlying disease process is suggested by these findings?
Diabetes mellitus. Proteinuria occurs in about half of patients with either type I or type II diabetes mellitus, usually about 1 to 2 decades after initial appearance of clinical diabetes mellitus, and suggests a greater likelihood for progression to chronic renal failure in 5 years.
- What additional laboratory testing would be helpful?
A fasting blood glucose greater than 140 mg/dl as measured on two occasions will document the hyperglycemia indicative of diabetes mellitus. The presence of ketonuria would suggest type I diabetes mellitus, but the lack of ketones is not specifically indicative of type II diabetes mellitus. If he were overweight, then type II is more likely.
- What other complications could be present, given his underlying disease? Examples of additional complications are shown in images 6.3 and 6.4.
Image 6.3 demonstrates numerous neutrophils in and around renal tubules, indicative of acute pyelonephritis. Image 6.4 shows many round cells, including lymphocytes, and more significantly, plasma cells, that can be found with chronic pyelonephritis. Urinary tract infections are more common and severe in patients with diabetes mellitus. Diabetics can also develop papillary necrosis. Accelerated atherosclerosis can lead to marked nephrosclerosis, either arterial or arteriolar. The term diabetic nephropathy is often used to denote the spectrum of pathologic lesions that can be found in kidneys in patients with diabetes mellitus types I and II.
- How would you deal with the complication of hypertension?
For persons with congestive heart failure or with diabetes mellitus type I and diabetic nephropathy, the angiotensin converting enzyme (ACE) inhibitors such as captopril, are recommended. Angiotensin-II receptor blockers, such as losartan, may be used in persons who cannot tolerate the ACE inhibitors and for those with type II diabetes mellitus.
The treatment of "essential" hypertension depends upon a variety of parameters, including the severity of the hypertension and the presence of other diseases. Persons with "high normal" pressures from 140-159/90-99 mm Hg (stage I hypertension), in the absence of other diseases, can be followed for 6 months to see if lifestyle changes, such as dietary modifications (reduction in salt intake) and exercise regimens with promotion of lifestyle modifications (stop smoking, lose weight) and having a pet (dog or cat) can aid in normalizing blood pressures in this range. If the hypertension persists after 6 months, then pharmacologic therapy is indicated.
Persons with pressures above 160/100 mm Hg (stage II hypertension) require immediate drug therapy. Initial therapy typically consists of diuretics and/or beta-adrenergic blockers, in the absence of any other diseases.
Diuretics aid in sodium excretion to reduce intravascular volume. The most common diuretics block sodium reabsorbtion and include the thiazides which act in the distal convoluted tubule, such as hydrochlorothiazide, and the loop diuretics, such as furosemide that act in the loop of Henle.
The beta blockers work by competitive inhibition of the effects of catecholamines on beta-adrenergic receptors. They can be cardioselective with primarilty beta-1 blocking effects, such as metoprolol, or non-selective with action on beta-2 receptors as well, such as propranolol.
Beta blockers are indicated for persons who have had a myocardial infarction. Such persons who cannot tolerate beta blockers may benefit from a calcium channel blocker such as diltiazem that causes arteriolar dilation.
Much higher blood pressures, or malignant hypertension, require more aggressive therapies, such as sodium nitroprusside which is a potent direct vasodilator.
- In patients with this disease, without hypertension, what pharmacologic agent(s) would be helpful? Which should be avoided?
An angiotensin converting enzyme (ACE) inhibitor is useful in slowing the progression of diabetic nephropathy in type I diabetes mellitus, even if all that is present is an early finding of microaalbuminuria, and angiotensin II receptor blockers in type II diabetes mellitus. Drugs to be avoided in persons with renal impairment include non-steroidal anti-inflammatory drugs (NSAIDS) and COX2 inhibitors, which inhibit prostaglandin synthesis. In normal kidneys, prostaglandins typically do not play a role in renal perfusion. However, with renal impairment the loss of the vasodilatory effect of prostaglandins can produce findings of prerenal azotemia.
- If the patient had undergone abdominal CT imaging with contrast, in order to investigate potential underlying conditions, and then developed acute renal failure, what issues would need to be addressed?
There is a potential risk for contrast-induced nephropathy. Though this is uncommon, increasing numbers of persons are receiving radiographic imaging studies with contrast.
If the issue is whether we should tell the patient his renal failure was caused by our treatment, and not try to pass it off as a complication of his underlying disease, the answer is yes. If it was caused by someone else's treatment, though, should we avoid laying blame on a colleague in our profession? Isn't that unprofessional? Isn't there something in the Hippocratic Oath about loyalty to the profession, meaning don't do things that will lead to liability? Well, no. Just as in the case of environmental exposures such as asbestos, the people who have been harmed deserve justice. Not only should we avoid concealing the truth, we should be obligated to tell the injured persons what we know.
Was it negligence? Not if it is a potential adverse event that is known and included in the informed consent process. Of course, if it is known and was not included in the informed consent process, then that is negligence. If an adverse event is an unexpected event, and was the result of a mistake in dosing or in asking the right questions or running the right test first, then it is also negligence.
