A Case Report of Premalignant Plasma Cell Dyscrasia-Induced Renal Failure in a 31-Year-Old Female.

Monoclonal gammopathy of renal significance (MGRS) is a rare disorder in which monoclonal immunoglobulin secreted by nonmalignant B cell or plasma cell clone causes kidney damage. Although MGRS is a premalignant condition, it can cause severe kidney disease and end-stage renal disease (ESRD) at any age. Herein, we present a 31-year-old female with past medical history of lupus nephritis who presented with signs of volume overload and worsening renal function despite adequate immunosuppressive therapy. Renal biopsy revealed heavy and light chain deposition consistent with MGRS. This case report demonstrates the importance of including MGRS in the differential diagnosis of worsening renal function despite adequate treatment, raising awareness of this premalignant yet morbid condition.

Bile Cast Nephropathy an Important Biliary Culprit of Kidney Injury.

Bile cast nephropathy (BCN) is a rare form of acute kidney injury (AKI) that occurs in the setting of hyperbilirubinemia. We present the case of a 67 year-old male with severe kidney injury who was found to have obstructive cholestasis. By way of this report, we aim to expand upon the existing literature and showcase the importance of timely endoscopic retrograde cholangio-pancreatography (ERCP) in this setting, in order to prevent irreversible kidney damage.

Myeloid-Derived Suppressor Cells Ameliorate Cyclosporine A-Induced Hypertension in Mice.

The calcineurin inhibitor cyclosporine A (CsA) suppresses the immune system but promotes hypertension, vascular dysfunction, and renal damage. CsA decreases regulatory T cells and this contributes to the development of hypertension. However, CsA's effects on another important regulatory immune cell subset, myeloid-derived suppressor cells (MDSCs), is unknown. We hypothesized that augmenting MDSCs would ameliorate the CsA-induced hypertension and vascular and renal injury and dysfunction and that CsA reduces MDSCs in mice. Daily interleukin-33 treatment, which increased MDSC levels, completely prevented CsA-induced hypertension and vascular and renal toxicity. Adoptive transfer of MDSCs from control mice into CsA-treated mice after hypertension was established dose-dependently reduced blood pressure and vascular and glomerular injury. CsA treatment of aortas and kidneys isolated from control mice for 24 hours decreased relaxation responses and increased inflammation, respectively, and these effects were prevented by the presence of MDSCs. MDSCs also prevented the CsA-induced increase in fibronectin in microvascular and glomerular endothelial cells. Last, CsA dose-dependently reduced the number of MDSCs by inhibiting calcineurin and preventing cell proliferation, as other direct calcineurin signaling pathway inhibitors had the same dose-dependent effect. These data suggest that augmenting MDSCs can reduce the cardiovascular and renal toxicity and hypertension caused by CsA.

Utility of Analgesic and Anxiolytic Medication Dose during Colonoscopy in Identifying Patients with Irritable Bowel Syndrome.

Research question. This paper was done to answer the question on whether patients with IBS require higher analgesic or anxiolytic doses during colonoscopy. Setting. Gastroenterology practice in Michigan, USA. Methods. We reviewed the charts of patients following up with a US based gastroenterology practice. We collected data on whether or not they had IBS, and collected data on analgesic and anxiolytic requirement during colonoscopy. Results. 336 patients were included in the trial. 206 did not have IBS while 130 had a previous diagnosis of IBS. 234 were female (67.2%). When comparing patients who have IBS to those without IBS, we identified no statistically significant difference in midazolam dose (5.5 mg versus 5.5 mg), fentanyl dose ( 117 mg versus 112 mg) or meperidine dose (69 mg versus 69 mg). The lack of differences in medication doses used remained when we controlled for sex, prior analgesic use, and prior abdominal surgery. Conclusion. Dose of analgesic or anxiolytic used during colonoscopy cannot be used to identify patients with IBS.

Pontine stroke presenting as isolated facial nerve palsy mimicking Bell's palsy: a case report.

INTRODUCTION: Isolated facial nerve palsy usually manifests as Bell's palsy. Lacunar infarct involving the lower pons is a rare cause of solitary infranuclear facial paralysis. The present unusual case is one in which the patient appeared to have Bell's palsy but turned out to have a pontine infarct. CASE PRESENTATION: A 47-year-old Asian Indian man with a medical history of hypertension presented to our institution with nausea, vomiting, generalized weakness, facial droop, and slurred speech of 14 hours' duration. His physical examination revealed that he was conscious, lethargic, and had mildly slurred speech. His blood pressure was 216/142 mmHg. His neurologic examination showed that he had loss of left-sided forehead creases, inability to close his left eye, left facial muscle weakness, rightward deviation of the angle of the mouth on smiling, and loss of the left nasolabial fold. Afferent corneal reflexes were present bilaterally. MRI of the head was initially read as negative for acute stroke. Bell's palsy appeared less likely because of the acuity of his presentation, encephalopathy-like imaging, and hypertension. The MRI was re-evaluated with a neurologist's assistance, which revealed a tiny 4 mm infarct involving the left dorsal aspect of the pons. The final diagnosis was isolated facial nerve palsy due to lacunar infarct of dorsal pons and hypertensive encephalopathy. CONCLUSION: The facial nerve has a predominant motor component which supplies all muscles concerned with unilateral facial expression. Anatomic knowledge is crucial for clinical localization. Bell's palsy accounts for around 72% of facial palsies. Other causes such as tumors and pontine infarcts can also present as facial palsy. Isolated dorsal infarct presenting as isolated facial palsy is very rare. Our case emphasizes that isolated facial palsy should not always be attributed to Bell's palsy. It can be a presentation of a rare dorsal pontine infarct as observed in our patient.