Impact of the Libby Zion case on graduate medical education in internal medicine.

Residency training in New York State was substantially altered by the Libby Zion case. Work-hour limitations and augmented supervisory requirements changed the patterns of training--particularly in internal medicine--but with uncertain impacts on the quality of education and patient care. In this historical analysis, we review another major effect of the case: a substantial augmentation of the number of trainees. The need to maintain adequate inpatient staffing--within the ground rules of the Residency Review Committee, and in consideration of the reimbursement formulae and financial climate of New York State--conspired to promote substantial residency program expansion. Similar forces contributed to a national trend to increase the number of trainees. The history, cost and impact of these personnel changes are reviewed.

Impaired renal vasodilation and urinary cGMP excretion in Dahl salt-sensitive rats.

We previously have shown that Dahl salt-sensitive rats increase renal vascular resistance in response to excessive salt feeding before total peripheral resistance increases and hypertension occurs. Failure of renal vasculature to dilate, as normally occurs in Dahl salt-resistant rats fed a high salt diet, may play a role in the development of hypertension in Dahl salt-sensitive rats. We also showed that renal vasculature in salt-sensitive rats is hyperreactive to vasoconstrictors and hyporeactive to vasodilators. Atrial natriuretic peptide, by stimulating cell-bound receptors, and nitroprusside, by generating nitric oxide, cause renal vasodilation by generating cGMP. Studies were undertaken to determine whether defective renal vasodilation in Dahl salt-sensitive rats is due to impaired production of cGMP. We examined the influence of nitroprusside infusion and salt intake on renal vascular resistance and cGMP excretion in salt-sensitive rats. Results demonstrate that salt feeding and nitroprusside infusion increase cGMP excretion and decrease renal vascular resistance in salt-resistant rats (P < .01), and, although this relationship was less clear in salt-sensitive rats, there was a reciprocal relationship between renal vascular resistance and cGMP excretion in all animals studied. Salt feeding and nitroprusside infusion caused less of an increase in cGMP excretion in salt-sensitive than in salt-resistant rats (P < .01). In conclusion, these studies support the concept that impairment in cGMP generation may play a primary role in the inability of the kidneys of Dahl salt-sensitive rats to vasodilate in response to increased salt intake. Such an impairment could contribute to salt retention and the development of hypertension.

How--and when--to obtain consent for do-not-resuscitate orders. Clinical guidelines and strategies for resolving conflicts.

Consider a do-not-resuscitate (DNR) order when a patient's presumed consent for cardiopulmonary resuscitation (CPR) is in question, the patient has an illness that is terminal or severe and irreversible, or he or she is permanently unconscious or likely to have cardiac or respiratory arrest. The patient with decisional capacity has the right to give or withhold consent for a DNR order. State law may limit a surrogate's authority to request that CPR be withheld. Remember, a DNR order does not restrict a patient's access to intensive care. Nurses, patient advocates, social workers, and clergy members may help mediate disputes. If necessary, seek advice from an ethics committee on how to resolve the conflict.

Using advance directives effectively in the intensive care unit. Terminating care in the presence--or absence--of directives.

When a patient is admitted to the ICU, determine whether the person has decisional capacity and whether an advance directive exists. If so, discuss treatment options and the directive with the patient--as well as with family members and appointed surrogates; clarify the patient's wishes. If no directive has been drawn up, encourage the patient to do so. If a patient lacks decisional capacity but has a directive, determine whether it applies to the current situation. If it does, follow its instructions. If no directive exists or if it does not apply, consult with family members to determine the patient's wishes, and ascertain whether these substitute judgments meet state laws.

How to determine decisional capacity in critically ill patients. Presume the patient can make decisions unless proven otherwise.

Decisional capacity includes ability to comprehend information, to make an informed choice, and to communicate that choice; it is specific to the decision at hand. Presume a patient has decisional capacity; an evaluation of incapacity must be justified. Administer a standardized mental status test to help assess alertness, attention, memory, and reasoning ability. A patient scoring below 10 on the Folstein Mini-Mental State Examination (maximum score, 30) probably does not have decisional capacity; one scoring from 10 to 15 probably can designate a proxy but not make complex health care decisions. Obtain psychiatric consultations for a patient who exhibits psychological barriers to decision making.

Posthysteroscopic hyponatremia.

We report a case of severe hyponatremia following hysteroscopic myomectomy for uterine fibroids. This new technique, which requires large volumes of irrigation solution (1.5% glycine in this case), is being more widely applied as an alternative to open surgery. Thus, nephrologists may expect to encounter such cases as the female counterpart to transurethral resection of prostate-associated hyponatremia. Analysis of the dynamic features of this case, in the context of recent knowledge of glycine metabolism, suggests that the early severe hyponatremia is partly spurious, reflecting an osmotic effect of glycine (which is initially restricted to the extracellular space). As glycine progressively enters cells and is metabolized, the later phase of hyponatremia more accurately reflects true hypo-osmolality.

Update on renal transplantation.

Renal transplantation has evolved as a preferred mode of long-term therapy for a substantial percentage of chronic renal failure patients. The author reviews recent progress in the field with an emphasis on patient counseling and with the conclusion that the outlook for these patients is bright.

Impaired renal vascular reactivity in prehypertensive Dahl salt-sensitive rats.

We have previously shown that renal vascular resistance is less in Dahl salt-sensitive rats than salt-resistant rats fed 1% NaCl diets; however, renal vascular resistance increases before nonrenal vascular resistance as salt-sensitive rats develop hypertension when fed 8% NaCl diets. When salt-resistant rats are given 8% NaCl diets, renal vascular resistance decreases. The current study reports effects of atrial natriuretic peptide, nitroprusside, norepinephrine, angiotensin II, and endothelin-1 on renal and nonrenal vascular resistance in prehypertensive salt-sensitive and salt-resistant rats given 1% NaCl diets; doses used did not affect blood pressure. Resistance of nonrenal vessels in salt-sensitive and salt-resistant rats responded similarly to dilators or constrictors. However, atrial natriuretic peptide and nitroprusside decreased renal vascular resistance of salt-resistant rats (by 65%, p less than 0.01) but not that of salt-sensitive rats. Norepinephrine, angiotensin II, and endothelin-1 increased renal vascular resistance in salt-sensitive rats by 126%, 135%, and 135%, respectively (p less than 0.01); norepinephrine and angiotensin II did not change renal vascular resistance of salt-resistant rats, but endothelin-1 decreased renal vascular resistance in salt-resistant rats by 30% (p less than 0.01). Reactivity of nonrenal blood vessels in prehypertensive salt-sensitive and salt-resistant rats was similar when infused with dilators or constrictors in doses used. By contrast, renal vessels of salt-sensitive rats did not dilate in response to atrial natriuretic peptide and nitroprusside but were hypersensitive to norepinephrine and angiotensin II. Endothelin-1 caused renal vasoconstriction in salt-sensitive rats and renal vasodilation in salt-resistant rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Soluble HLA antigens, anti-HLA antibodies, and antiidiotypic antibodies in the circulation of renal transplant recipients.

Chronic rejection represents the major threat to long-term survival of organ allografts. It is presumed that this form of rejection is mediated by antibodies against mismatched HLA antigens of the graft. The presence and specificity of anti-HLA-antibodies in posttransplantation sera are, however, difficult to document. We have explored the possibility that anti-HLA antibodies form immune complexes with soluble HLA antigens released from the injured graft and/or that they are blocked by antiidiotypic, anti-anti-HLA-antibodies. Our data demonstrate that the long-term survival of renal allografts is significantly lower in patients who develop anti-HLA-antibodies following transplantation than in patients who do not form antibodies. Following depletion of soluble HLA antigens by magnetic immunoaffinity, we could identify anti-HLA-antibodies in 57% of the sera obtained from patients undergoing chronic rejection of kidney allografts, compared with 41% prior to antigen depletion. In patients tolerating the graft for 4 years or more, the corresponding frequencies of antibody-positive sera was 2% and 5% prior and following depletion of HLA antigens. The presence of HLA antigen/anti-HLA-antibody immune complexes in patients' sera was positively associated with chronic humoral rejection (P less than 0.0001). Patients who tolerated the graft in spite of having developed antibodies against one of its mismatched HLA antigens show specific antiidiotypic (anti-anti-HLA-antibodies). Such antiidiotypic antibodies were not found in sera from patients with chronic rejection (P = 0.005). This indicates that antiidiotypic antibodies may delay the progression of chronic humoral rejection.

Tuberculous peritonitis in a CAPD patient cured without catheter removal: case report, review of the literature, and guidelines for treatment and diagnosis.

Tuberculous peritonitis in the chronic peritoneal dialysis patient carries a high mortality, which may reflect the diagnostic delay that is often encountered in these cases. Accordingly, a high index of suspicion and an aggressive diagnostic approach (which may include laparoscopic biopsy) should be applied to the patient with persistent culture negative peritonitis. One of the first continuous ambulatory peritoneal dialysis (CAPD) cases involving tuberculous peritonitis successfully treated without interruption of dialysis or removal of the peritoneal dialysis catheter is reported. The literature is reviewed to provide diagnostic and therapeutic guidelines in dealing with this serious infection.

Recurrent IgA nephropathy in living-related donor transplantation: recurrence or transmission of familial disease?

We describe a patient who developed terminal renal failure of two HLA-identical renal allografts due to crescentic IgA nephropathy. The first graft contained IgA deposits at the time of donation, suggesting that transmission of IgA deposits may have contributed to the nephritis of the first allograft. The second graft was free of IgA deposits at the time of donation, but the recipient developed a similar, rapidly progressive nephritis. This case points up the malignant potential of IgA nephropathy and the complex nature of transplant planning for patients with end-stage renal disease (ESRD) secondary to IgA nephropathy. Living-related donor (LRD) transplants seem to be associated with a higher rate of recurrence than cadaveric grafts. This higher rate may partly reflect the inadvertent transmission of subclinical IgA deposits from donor to recipient and a genetic susceptibility of certain HLA types (specifically B35 and DR4) to recurrent disease. Cadaveric transplants may be preferable in the setting of high-risk HLA types or familial patterns of IgA nephropathy.