Meningitis admitted to a military hospital: a retrospective case series.

Meningitis is a common admission diagnosis. No case series or descriptive studies on meningitis have recently been published. Additionally, no recent data exist on meningitis in the U.S. Military Health System. We reviewed charts of adult patients admitted to Naval Medical Center San Diego between January 2004 and December 2008 with an admission diagnosis of meningitis. Charts were excluded if they did not meet our case definition of meningitis, if missing data, or if meningitis was nosocomial or iatrogenic. We reviewed results of cerebrospinal fluid cultures during this period. We compared rates and characteristics, and outcomes of bacterial and aseptic meningitis. Two hundred twenty-one cases met our criteria. Of these, 208 were aseptic. Cerebrospinal fluid polymerase chain reaction testing was positive for enteroviruses and herpes simplex viruses in 42 (20.2%) and 17 (8.2%) cases, respectively. Of culture/polymerase chain reaction/serologically positive cases, the pathogens were Neisseria meningitidis (3), Streptococcus pneumoniae (3), viridans streptococci (2), Cryptococcus neoformans (2), Coccidioides immitis (2), and Mycobacterium tuberculosis (1). Three patients had poor outcomes: one died from S. pneumoniae and two had long-term neurologic deficits. Meningitis is a common admission diagnosis, but serious virulent pathogens are uncommon and adverse outcomes are rare.

Squamous cell carcinoma in situ arising at the exit site of a tunneled catheter.

Squamous cell carcinoma (SCC) is a well-known complication of immunosuppression associated with organ transplantation. It may arise de novo or from previously existing in situ lesions (Bowen's disease). Concurrent human papilloma virus infection often has an etiologic role, and SCC may follow an aggressive course in immunosuppressed patients. The authors describe a liver transplant patient in whom end-stage renal disease developed. She underwent tunneled catheter placement followed by arteriovenous graft placement. Subsequently, a large SCC in situ at the exit site of her prior tunneled hemodialysis catheter occurred. The growth was removed surgically without complication. SCC has not been reported previously to arise from a catheter exit site. This entity is common in renal and other transplant populations and may follow an aggressive course. It should be sought out by careful skin evaluation to include areas not routinely exposed to the sun.

Early diabetes as a model for testing the regulation of juxtaglomerular NOS I.

Dysregulation of kidney nitric oxide synthase (NOS) I may alter renal hemodynamics in diabetes. Four types of studies were performed in anesthetized 1- to 2-wk-streptozotocin diabetic rats. 1) Glomerular filtration rate (GFR) was measured before and during NOS I blockade. Subsequent addition of nonspecific NOS blocker tested for residual NO from other isoforms. Acute systemic NOS I blockade reduced GFR only in diabetics. Nonspecific NOS blockade had no additional effect on NOS I-blocked diabetics. 2) Renal blood flow (RBF) was monitored for evidence that tubuloglomerular feedback (TGF) resets during 1 h of continuous activation with benzolamide. NOS I blockade was added to test for the role of NOS I in TGF resetting. During 1 h of TGF activation in controls, RBF initially declined and then returned to baseline. In diabetic and NOS I-blocked rats, RBF declined and remained low. 3) The ability of NOS I blockade to increase the homeostatic efficiency of TGF in diabetes was tested by micropuncture in free-flowing nephrons. The addition of NOS I blocker to the tubular fluid increased TGF efficiency in control and diabetic rats. 4) The influence of distal salt delivery on local NOS I activity was tested by micropuncture. Henle's loop was perfused at varying rates with NOS I blocker while single-nephron GFR (SNGFR) from the late proximal tubule was measured. In controls, NOS I blockade mainly reduced SNGFR when flow through Henle's loop was high. In diabetics, NOS I blockade reduced SNGFR independently of flow through Henle's loop. In conclusion, normally, salt delivered to the macula densa (MD) exerts immediate control over MD NOS I activity. In diabetes, there is ongoing overactivity of NOS I that is not regulated by MD salt.

Hemodynamics of early tubuloglomerular feedback resetting during reduced proximal reabsorption.

BACKGROUND: Carbonic anhydrase inhibition with benzolamide reduces proximal reabsorption and activates tubuloglomerular feedback (TGF). In rats, TGF activation for 30 to 60 minutes locally suppresses renin secretion and resets TGF rightward to accommodate increased late proximal flow. After 24 hours of TGF activation, there is upward resetting of GFR and increased activity of macula densa nitric oxide synthase I (NOS I). METHODS: We studied renal hemodynamics during early TGF resetting with attention to the importance of renin suppression and NOS I activation. Left kidney blood flow (RBF, pulse Doppler) and glomerular filtration rate (GFR; inulin clearance or Fick method) were measured before and during benzolamide infusion (5 mg/kg bolus followed by 5 mg/kg/h IV) in Wistar rats concurrently receiving the converting enzyme inhibitor, enalaprilat (0.3 mg/kg/h IV) or NOS-I blocker S-methyl-thiocitrulline (SMTC; 2.7 mg/kg/h IV). RESULTS: Activating TGF initially reduced RBF and GFR in all groups as expected. During continuous benzolamide, RBF gradually increased toward baseline in control and enalaprilat-treated rats, but not in NOS I-blocked rats. After the initial decline, GFR did not change further during one hour of benzolamide in any group. CONCLUSIONS: During one hour of persistent TGF stimulation, RBF increases toward normal, but GFR does not. This requires an overall decrease in renal vascular resistance and a decrease in the ratio of efferent/afferent arteriolar resistance (RE/RA), implying a major decrease in RE. NOS I, but not angiotensin-converting enzyme (ACE), is required for RBF to increase during TGF resetting. Although the hemodynamic changes during TGF resetting resemble the response to blocking the renin-angiotensin system, these data fail to show that the increase in RBF during early TGF resetting is mediated by renin suppression.

Glomerulotubular balance, dietary protein, and the renal response to glycine in diabetic rats.

The glomerular filtration rate (GFR) normally increases during glycine infusion, which is a test of "renal reserve." Renal reserve is absent in diabetes mellitus. GFR increases after protein feeding because of increased tubular reabsorption, which reduces the signal for tubuloglomerular feedback (TGF). Dietary protein restriction normalizes some aspects of glomerular function in diabetes. Renal micropuncture was performed in rats 4-5 wk after diabetes was induced by streptozotocin to determine whether renal reserve is lost as a result of altered tubular function and activation of TGF, whether 10 days of dietary protein restriction could restore renal reserve, and whether this results from effects of glycine on the tubule. TGF activation was determined by locating single-nephron GFR (SNGFR) in the early distal tubule along the TGF curve. The TGF signal was determined from the ionic content of the early distal tubule. In nondiabetic rats, SNGFR in the early distal tubule increased during glycine infusion because of primary vasodilation augmented by increased tubular reabsorption, which stabilized the TGF signal. In diabetic rats, glycine reduced reabsorption, thereby activating TGF, which was largely responsible for the lack of renal reserve. In protein-restricted diabetic rats, the tubular response to glycine remained abnormal, but renal reserve was restored by a vascular mechanism. Glycine affects GFR directly and via the tubule. In diabetes, reduced tubular reabsorption dominates. In low-protein diabetes, the vascular effect is enhanced and overrides the effect of reduced tubular reabsorption.