[Mononeuritis multiplex under the TNF-alpha inhibitor infliximab]. / Mononeuritis multiplex unter dem TNF-alpha-Hemmer Infliximab.

A 21-year-old patient with ankylosing spondylitis under treatment with the TNF-alpha inhibitor infliximab developed a multifocal, demyelinating axonal neuropathy affecting several peripheral nerves simultaneously (mononeuritis multiplex). This represents an additional rare peripheral nervous system side effect of infliximab therapy. The underlying cause is unknown. Intravenous immunoglobulin therapy (0.4 g/kg per day for five days) led to a complete regression of muscle paresis and sensory defects in this case.

Sodium homeostasis in transplanted rats with a spontaneously hypertensive rat kidney.

Recipients of a kidney from spontaneously hypertensive rats (SHR) but not from normotensive Wistar-Kyoto rats (WKY) develop posttransplantation hypertension. To investigate whether renal sodium retention precedes the development of posttransplantation hypertension in recipients of an SHR kidney on a standard sodium diet (0.6% NaCl), we transplanted SHR and WKY kidneys to SHR x WKY F1 hybrids, measured daily sodium balances during the first 12 days after removal of both native kidneys, and recorded mean arterial pressure (MAP) after 8 wk. Recipients of an SHR kidney (n = 12) retained more sodium than recipients of a WKY kidney (n = 12) (7.3 +/- 10 vs. 4.0 +/- 0.7 mmol, P < 0.05). MAP was 144 +/- 6 mmHg in recipients of an SHR kidney and 106 +/- 5 mmHg in recipients of a WKY kidney (P < 0.01). Modest sodium restriction (0.2% NaCl) in a further group of recipients of an SHR kidney (n = 10) did not prevent posttransplantation hypertension (MAP, 142 +/- 4 mmHg). Urinary endothelin and urodilatin excretion rates were similar in recipients of an SHR and a WKY kidney. Transient excess sodium retention after renal transplantation may contribute to posttransplantation hypertension in recipients of an SHR kidney.

The importance of the kidney in primary hypertension: insights from cross-transplantation.

Experimental renal cross-transplantation studies with genetically hypertensive and normotensive rats have shown that hypertension travels with the kidney. The underlying mechanisms are currently not well understood. Genetically normotensive recipients of a kidney from spontaneously hypertensive rats show a decreased capacity to excrete sodium when challenged with a high-salt diet. Furthermore, they retain more sodium than recipients of a kidney from genetically normotensive donors immediately after transplantation and removal of the native kidneys. Sodium retention precedes hypertension and may contribute to its development. Most recently, it has been shown that bilateral nephrectomy and transplantation of a genetically normotensive kidney attenuates the development of hypertension in young transplanted spontaneously hypertensive rats. Thus, long-term blood pressure in renal transplanted rats is critically determined by the genetic background of the renal graft. Together, these data indicate that genetically determined renal mechanisms play a major role in primary hypertension.