We report a case of a 71-year-old Filipino female who was admitted to the hospital for abdominal pain, vomiting and diarrhea of 8 days duration. The patient was found to have marked acute kidney injury (AKI), which required hemodialysis in the next 3 days. Extensive workup revealed hematuria, subnephrotic range proteinuria, elevated anti-nuclear antibody (ANA) and elevated total immunoglobulin G (IgG) levels, with normal IgG4 and anti-dsDNA levels. On kidney biopsy, mild membranous glomerulonephritis was found, along with autoimmune tubulointerstitial nephritis (TIN) with a “full-house” pattern of immune deposits. These findings were suggestive of lupus interstitial nephritis. However, IgG4+ plasma cells were detected in the interstitium by immunostaining, favoring a diagnosis of IgG4-related kidney disease (IgG4-RKD). Our case highlights the difficulty in differentiating lupus nephritis (LN) from IgG4-RKD in some patients, raising the suspicion that these two entities can co-exist.
Immunoglobulin D (IgD) multiple myeloma (MM) is a very rare form of myeloma affecting less than 2% of all myeloma patients. It has a multiorgan involvement with renal failure being the key feature. We present here a case of IgD MM in a 62-year-old white male, smoker with past medical history of hypertension, who presented to emergency department with complaints of lower abdominal pain, constipation and decreased urination. Physical exam was unremarkable. Laboratory investigation showed S.Cr 5.99 mg/dL, hemoglobin 8.7 g/dL and corrected S.Ca 10.6 mg/dL. Urine dipstick showed 100 protein and TP/Cr ratio was 23. Serology was positive for serum free lambda chain level of 8,947.6 mg/L as well with free κ/λ ratio < 0.01. The results of serum and urine electrophoresis and immunofixation were also supportive of diagnosis of IgD MM. IgD level was remarkably elevated (27,300 mg/L) too. CT scan of abdomen/pelvis was negative for obstructive uropathy. Skeletal survey showed a solitary lytic lesion in the iliac crest. His kidney function deteriorated next day requiring hemodialysis. The bone marrow biopsy was positive for plasma cell hypercellularity (70-80%) and flow cytometry showed 8% monoclonal IgD lambda plasma cells. The patient was started on bortezomib and dexamethasone and he underwent bone marrow transplant 6 months later. He is doing well hematologically now but he remains dialysis-dependent. IgD MM is a very rare disease affecting younger population with poor prognosis; patients often end up on hemodialysis despite better control of the hematological component.
The potential for splenic injury from esophagogastroduodenoscopy (EGD) is exceptionally low. To our knowledge, less than five cases have been reported in literature. Though still uncommon, splenic rupture due to diagnostic or therapeutic procedures is more frequently described following colonoscopy and endoscopic retrograde cholangiopancreatography. We report a 62-year-old Caucasian male with primary squamous cell carcinoma of the lung who presented 2 days after an EGD and gastric ulcer biopsy. The patient complained of severe left upper quadrant abdominal pain with rebound tenderness. Upon further evaluation, a diagnosis of a large subcapsular splenic hematoma was made with computed tomography (CT) imaging. The mechanism of splenic injury attributable to EGD is traction on the greater curvature of the stomach, causing avulsion of the splenic or short gastric vessels. We feel this case represents a very rare yet serious complication of EGD that warrants consideration and further investigation.
Serotonin syndrome is a potentially fatal increase in serotonergic activity in both the central nervous system and peripheral nervous system. The etiology can vary from therapeutic drug use, deliberate overdose or drug interactions that all lead to an increase in serotonin activity. There are a number of drugs from different classes that can cause serotonin syndrome either alone at high doses or when combined. We present here a case of a 74-year-old Caucasian female that presented to the emergency room with altered mental status, tachypnea, tachycardia and agitation. She reported taking her usual escitalopram as well as tramadol given to her by a friend to alleviate a headache. She was found tachycardic with a fever of 102.9 °F. She very quickly became combative and had to be sedated and intubated. Laboratory test results were remarkable for severe rhabdomyolysis for which she was treated aggressively with hydration. The patient was extubated on the fifth day after admission once her vitals were stable. Unfortunately, she then developed an intracranial bleed. She was ultimately transferred to another facility with the expectation of being evaluated by a neurosurgeon for the bleed. This patient was diagnosed with serotonin syndrome.
Calciphylaxis or calcific uremic arteriolopathy (CUA) is a rare disorder of calcium and phosphate metabolism most often manifesting in end-stage renal disease (ESRD) patients. The typical clinical picture is that of a necrotic cutaneous ulceration with focal or diffuse distribution, most often manifesting on the lower extremities. We report a 49-year-old Caucasian male with ESRD on hemodialysis who presented to the emergency department with complaints of lower extremity pain and multiple cutaneous necrotic lesions on his lower extremities. Patient reports seeking assistance from several medical providers over a 3-month period. Upon admission and further evaluation, a diagnosis of calciphylaxis was made clinically and confirmed by a skin biopsy. Sodium thiosulfate was initiated and the clinical picture improved significantly. Sodium thiosulfate is traditionally used as an antidote for cyanide poisoning, and it has demonstrated beneficial outcomes in most patients afflicted with CUA. The rationale behind sodium thiosulfate therapy in CUA is its role in chelating calcium into calcium thiosulfate, which increases its solubility leading to improved renal clearance. It is essential to raise awareness amongst physicians and medical practitioners alike, as early recognition and initiation of appropriate treatment can improve the patients' quality of life and more importantly, decrease mortality.
We report a case of a 48-year-old male who presented with hematuria of at least 10 years, and has a daughter with hematuria as well. The patient has a history of degenerative hearing loss, decreased vision and cataract formation, but no diabetes, hypertension or proteinuria. A full serology and urology workup was negative for any abnormality. A kidney biopsy for the patient revealed a diagnosis of Alport syndrome but was unable to rule out thin basement membrane disease. The biopsy was inconclusive in making the diagnosis but the patient’s clinical presentation led to the diagnosis of Alport syndrome. The patient’s 10-year-old daughter also has hematuria with no clear etiology but now can subsequently be anticipatorily managed for Alport syndrome progression. Due to the rarity of the disease, diagnosis is often missed or delayed by primary care providers especially when no associated proteinuria has yet developed. This can lead to confusion and misdiagnosis with thin basement membrane disease, a generally benign hematuria without kidney failure progression. Additionally, biopsy can be inconclusive in these patients, relying on the physician’s history and physical examination findings to diagnose. It is important to appropriately diagnose Alport syndrome not only to manage the patient’s rate of kidney failure progression but also allow for a higher degree of suspicion, screening and intervention in the patient’s family members. Both the inconclusive nature of kidney biopsies and the usefulness of diagnosis for family member screening are often overlooked in medical literature but are explored in this case.
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