We report a case of a patient presenting with a triad of hypercalcemia, metabolic alkalosis and renal failure secondary to calcium bicarbonate intake for osteoporosis prevention. It is the classical presentation of the “modern” milk alkali syndrome that presents several characteristics distinguishing it from the “old” syndrome described secondary to peptic ulcer disease treatment. Milk alkali syndrome affects middle-aged female patients taking over-the-counter calcium carbonate. Clinically, these patients present in an acute hypercalcemia crisis, responding rapidly to hydration. The phosphorus level is normal to low. Bisphosphonate should be used cautiously due to the risk of symptomatic hypocalcemia.
IntroductionWe present a case of pyelovenous backflow after nephrostomy. To the best of our knowledge, this is the first documented case of renal vein visualization after a nephrostomic placement.Case presentationA 55-year-old Caucasian man presented with symptoms of pyelonephritis with an obstructing ureteral stone. A nephrostomy was performed. During an injection of contrast agent in his left caliceal system, his left renal vein was visualized. A repeat pyelography with an injection contrast material at low pressure failed to show the same finding. This radiological finding is due to the occurrence of "pyelovenous backflow".ConclusionThis phenomenon is usually described in the setting of renal vein thrombosis, renal vein hypertension due to the "nutcracker phenomenon", or a reduced renal blood flow. Examination by microscopy shows the presence of tears in the fornix of the pelvic cavity that extend into the kidney parenchyma. Five types of renal backflow are described in the literature: pyelovenous, pyelolymphatic, pyelotubular, pyelointerstitia and pyelosinus. Injection of contrast material at high pressure may cause a fornix to flow into the tubules, or cause its rupture and flow into the venous system.
IntroductionLaboratory tests play a central role in assessing a patient and orienting the diagnostic evaluation. We report a case where the discrepancy between the manual and automatic cell count gave a hint to the final diagnosis.Case presentationA 55-year-old Caucasian man, known to have hepatitis C, was admitted with acute respiratory failure secondary to acute pulmonary edema and diffuse petechial rash of the lower extremities for the previous 2 months. The initial laboratory tests showed acute renal failure (creatinine of 2.6 mg/dL). During his hospital stay, the patient had a fluctuating white blood cell count with a recorded value of 96,000 cells/mL. On a peripheral smear, the blood cell count was in the normal range. The acute renal failure was secondary to membranoproliferative glomerulonephritis secondary to essential mixed cryoglobulinemia diagnosed by biopsy. The complete blood count values, performed by Beckman/Coulter GenS, were falsely high due to precipitation of plasma cryoglobulins at room temperature. This spurious leukocytosis was previously described in several case reports, but values as high as 96,000 cells/mL were never reported.ConclusionThe presence of cryoglobulins in the blood creates a clinical challenge for the interpretation of several laboratory tests. Pseudoleukocytosis secondary to cryoglobulinemia has been observed in several reported cases with white blood cell counts up to 54,000 cells/mL at room temperature and 85,600 cells/mL at 4°C. If the cryoglobulin precipitates rapidly, aggregated cryoglobulin particles may be interpreted as blood cells. We report the first patient with pseudoleukocytosis secondary to hepatitis C cryoglobulinemia with a spurious leukocytosis of 96,000 cells/mL at room temperature. Other laboratory tests could also be affected: underestimation of true erythrocyte sedimentation rate, pseudothrombocytosis and pseudolymphocytosis. The precipitation can remove the hepatitis C virus and the antibody of cryoglobulins from serum leading to a false negative result. Any discrepancy between the automated and manual white blood cell count should lead to the suspicion of cryoglobulinemia in the clinical setting.
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