Sustained hyperkalemia in an asymptomatic primary care patient. When to suspect familial pseudohyperkalemia.

Objectives: Study and management of a case with elevated potassium levels without apparent clinical causes in successive follow-up visits. Case presentation: We present the case of a primary care female patient who persistently exhibited elevated levels of potassium (5.3-5.9 mmol/L) in successive control laboratory tests, without an apparent clinical cause. The patient was ultimately referred to the Unit of Nephrology, where a potassium-low diet was indicated. Diet did not have any effect on potassium levels. After a thorough study, the cause of hyperkalemia could not be determined. Conclusions: The inconsistency between elevated potassium levels and the reason of consultation, and exclusion of other pre-analytical or pathological causes raised suspicion of familial pseudohyperkalemia. The sample was incubated at different times and temperatures to demonstrate their influence on levels of potassium in blood. Familial pseudohyperkalemia was established as the most probable diagnosis. Finally, the patient was discharged from the Unit of Nephrology and instructed to follow a normal diet.

Seudohiperfosfatemia analítica como punto de partida en el diagnóstico de una disproteinemia / Role of pseudo-hyperphosphataemia in the diagnosis of dysproteinaemia

El fósforo es el segundo mineral más abundante en el organismo. Su homeostasis se consigue mantener a través de varios mecanismos mediados principalmente por el riñón, el intestino y el hueso. Se han descrito interferencias en la medición del fósforo que pueden provocar una seudohiperfosfatemia. La causa más frecuente es la presencia de una paraproteína en el suero de los pacientes con mieloma múltiple, macroglobulinemia de Waldenström y gammapatía monoclonal de significado incierto. En los casos de hiperfosfatemia sin causa aparente que la pueda justificar, es importante tener en cuenta la existencia de una seudohiperfosfatemia causada por la presencia de las paraproteínas en sangre en los autoanalizadores de química líquida. El sistema multicapa de Vitros(R) 5600 es un método rápido y fiable para solucionar este problema

Phosphorus is the second most important mineral in the body. Its homeostasis is maintained through several mechanisms mediated mainly by the kidney, intestine, and bone. Interferences have been described in the measurement of phosphorus that could suggest a pseudo-hyperphosphataemia. The most frequent cause was the presence of a paraprotein in the serum of patients with multiple myeloma, Waldenström macroglobulinaemia, or monoclonal gammopathy of uncertain significance, was described as the most frequent cause of interference in phosphorus assay using liquid chemistry autoanalysers. When hyperphosphataemia is present, and no apparent cause can justify it, it is important to consider the possibility of a pseudo-hyperphosphataemia caused mainly by the presence of a paraprotein. The Vitros(R) 5600 multilayer system can be used as a fast and reliable method to avoid this interference

Participation of the dentate-rubral pathway in the kindling model of epilepsy.

Lesions of the cerebellar dentate nucleus (DN) reduce the after-discharge duration induced by repetitive kindling stimulation and decrease seizures to a lower rank according to Racine's scale. The DN sends cholinergic and glutamatergic fibers to the red nucleus (RN), which is composed of glutamatergic and GABAergic cells. To test the participation of these neurotransmitters in seizures, we compared the levels of glutamate and gamma-aminobutyric acid (GABA) at the RN in a control condition, a kindled stage, and a kindled stage followed by DN lesions. We found that the kindled stage was associated with significant reductions in glutamate and GABA in the RN and that the lesions of the DN in kindled rats reversed the severity of seizures and restored the GABA levels. GAD65 , a GABA-synthesizing enzyme, was increased in kindled rats and decreased after DN lesions. GAD65 commonly appears localized at nerve terminals and synapses, and it is only activated when GABA neurotransmission occurs. Thus, it is possible that the increased expression of GAD65 found in kindled rats could be due to an exacerbated demand for GABA due to kindled seizures. It is known that GABA maintains the inhibitory tone that counterbalances neuronal excitation. The decreased expression of GAD65 found after the DN lesions indicated that the GABA-synthesizing enzyme was no longer required once it eliminated the excitatory glutamate input to the RN. We thus conclude that DN lesions and their consequent biochemical changes are capable of decreasing the generalized seizures induced by kindling stimulation. © 2016 Wiley Periodicals, Inc.