Laboratory interpretative comments and guidance: clinical and operative outcomes on moderate to severe hyponatraemia patient management.

AIMS: Hyponatraemia is the most common body fluid disorders but often goes unnoticed. Our laboratory incorporated a standardised procedure to help clinicians detect moderate/severe hyponatraemia. The study aims were to evaluate the outcomes on patient care and clinicians' satisfaction. METHODS: The study, observational and retrospective, included 1839 cases, adult and paediatric patients, with sodium concentration <130 mmol/L. The procedure consisted of interpretative comments in the emergency and core laboratories report and the point-of-care testing blood gas network report. We evaluated hyponatraemia length in two equal periods: before and after the implementation. We conducted a survey addressed to the staff of the clinical settings involved to know their satisfaction. RESULTS: The median hyponatraemia length decreased significantly from 4.95 hours (2.08-16.57) in the first period to 2.17 hours (1.06-5.39) in the second period. The lack of hyponatraemia patients follow-up was significantly less after the procedure implementation. The survey was answered by 92 (60 senior specialists and 32 residents) out of 110 clinicians surveyed. Ninety of them (98%) answered positively. CONCLUSIONS: We have demonstrated the reduction in the time for diagnosing and management by physicians, the higher uniformity in the time required to solve hyponatraemia episodes following our laboratory procedure and the clinicians' satisfaction.

SARS-CoV-2 infection associated with monoclonal gammopathy. A case report based on the study of minimally invasive ultrasound-guided autopsy.

Coronavirus disease-2019 (COVID-19) is a global public health emergency with numerous clinical facets, including acute kidney injury and acute cerebrovascular disease. Further knowledge of its various pathogenic mechanisms is essential, including coagulation disorders. Monoclonal gammopathy is characterized by the overproduction of a monoclonal immunoglobulin caused by clonal proliferation. Using a postmortem study of ultrasound-guided percutaneous core biopsies, the aim of this report is to present our observations on the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection pathology associated with monoclonal gammopathy. The clinical presentation was acute renal failure. Pathological findings revealed kappa light chain cast nephropathy. SARS-CoV-2 immunohistochemistry was positive in some renal tubular cells. Another notable finding was the presence of a high density of alveolar megakaryocytes, which probably explained the final outcome (acute cerebrovascular disease). Immunohistochemical study for SARS-CoV-2 does not verify the pathogenic effect of the virus and thus its contribution to the acute kidney injury.

SARS-CoV-2 infection associated with monoclonal gammopathy. A case report based on the study of minimally invasive ultrasound-guided autopsy

Coronavirus disease-2019 (COVID-19) is a global public health emergency with numerous clinical facets, including acute kidney injury and acute cerebrovascular disease. Further knowledge of its various pathogenic mechanisms is essential, including coagulation disorders. Monoclonal gammopathy is characterized by the overproduction of a monoclonal immunoglobulin caused by clonal proliferation. Using a postmortem study of ultrasound-guided percutaneous core biopsies, the aim of this report is to present our observations on the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection pathology associated with monoclonal gammopathy. The clinical presentation was acute renal failure. Pathological findings revealed kappa light chain cast nephropathy. SARS-CoV-2 immunohistochemistry was positive in some renal tubular cells. Another notable finding was the presence of a high density of alveolar megakaryocytes, which probably explained the final outcome (acute cerebrovascular disease). Immunohistochemical study for SARS-CoV-2 does not verify the pathogenic effect of the virus and thus its contribution to the acute kidney injury.(AU)

La enfermedad por coronavirus de 2019 (COVID-19) es una emergencia sanitaria pública global con numerosas facetas clínicas que incluyen enfermedad renal aguda y enfermedad cerebrovascular aguda. Es necesario un conocimiento adicional de su mecanismo patogénico. Los trastornos de coagulación están claramente incluidos en dichos mecanismos. La gammapatía monoclonal se caracteriza por la sobreproducción de inmunoglobulina monoclonal causada por proliferación clonal. Utilizando un estudio postmortem de biopsias percutáneas ecoguiadas, el objetivo de este informe es presentar nuestras observaciones sobre la patología del síndrome respiratorio agudo severo por infección de coronavirus 2 (SARS-CoV-2) con gammapatía monoclonal. La presentación clínica fue insuficiencia renal aguda. Los hallazgos patológicos revelaron nefropatía por cilindros de cadenas ligeras kappa. La inmunohistoquímica de SARS-CoV-2 fue positiva en ciertas células tubulares renales. La presencia de megacariocitos alveolares (alta densidad) fue un hallazgo notable, que explica probablemente el resultado final del paciente (enfermedad cerebrovascular aguda). El estudio inmunohistoquímico frente a SARS-CoV-2 no verifica el efecto patogénico del virus y, por tanto, su contribución a la nefropatía aguda.(AU)

Goodpasture's syndrome associated with thrombotic thrombocytopenic purpura secondary to an ADAMTS-13 deficit.

A 27-year-old man was hospitalized for acute kidney injury associated with antiglomerular basement membrane antibodies (anti-GBM). He underwent immunosuppression and plasma exchange therapy, without recovery of renal function. Later on, he was again admitted to the hospital with seizures. Evidence of microangiopathic hemolytic anemia, with schistocytes in peripheral blood, was present, as well as a persistent low platelet count and activity of von Willebrand factor from adherence to protease (ADAMTS-13) less than 1 %. The presence of IgG antibodies against ADAMTS-13 was documented, leading to a diagnosis of thrombotic thrombocytopenic purpura (TTP) in the context of Goodpasture's syndrome. The TTP was treated with rituximab and plasmapheresis with a good response. We conclude that early measurement of ADAMTS-13 activity dictated the most appropriate therapy and achieved excellent results in this patient.

Thyroid function tests in acute kidney injury.

OBJECTIVE: The aim of this study was to analyze the prevalence, clinical significance and prognostic implications of alterations in thyroid function tests (TFTs) in patients with acute kidney injury (AKI). METHODS: A prospective study was carried out in patients hospitalized for AKI for 2 consecutive years. TFTs (serum thyrotropin [TSH], free thyroxine [FT4] and total triiodothyronine [T3] concentrations) were completed for each patient on 3 occasions: at admission, at hospital discharge and at their first outpatient visit. TFTs were related to clinical and analytical data. Thirty-five patients (16 women [45.7%], mean age ± SD, 65.2 ± 18.0 years) with AKI (creatinine 5.6 ± 2.2 mg/dL) were studied. There were 10 (28.6%), 10 (28.6%), 11 (31.4%) and 4 (11.4%) patients with prerenal, renal, mixed (prerenal and renal), and postrenal AKI, respectively. RESULTS: Total prevalence of alterations in TFTs was 82.9% (n=29). Of those, euthyroid sick syndrome (ESS) with low T3 only was the most common (n=13, 37.1%) derangement. In the whole group of patients, median TSH (0.93 µU/mL, interquartile range 0.35-2.27 µU/mL)and mean FT4 (1.2 ± 0.3 ng/dL) were normal, whereas mean T3 was low (0.7 ± 0.1 ng/mL). TSH, FT4 and T3 were similar in different types of AKI. On simple regression analysis, we found a negative correlation only between TSH and serum urea concentrations (ro=-0.382; p=0.024). At hospital discharge (median hospital stay 6 days; range 2-10 days), TFT showed significant changes only in T3 concentrations (0.8 ± 0.3 ng/mL, p=0.013). At this point, the percentage of patients with normal TFT increased from 17.1% at baseline to 40% at discharge and then to 66.7% at their first outpatient visit. We found no association between the presence and type of alterations in TFT and clinical factors (sex, age, personal history of diabetes and/or hypertension, number and type of drugs used, number of signs and symptoms at AKI diagnosis, and degree, type and cause of AKI) or prognostic factors (hospital stay, recovery of renal function, need for renal replacement therapy by hemodialysis, development and degree of residual chronic renal failure and mortality) associated with AKI. CONCLUSION: Over 80% of AKI patients exhibit alterations in TFT. The commonest derangement is ESS (~70%), mainly low T3 syndrome, which is present in about one third of the patients with altered TFT. ESS recovers spontaneously as renal function improves. The presence of TFT alterations seems to not be associated with clinical and prognostic implications in AKI patients.

Octreotide reduces hepatic, renal and breast cystic volume in autosomal-dominant polycystic kidney disease.

A 43-year-old woman with autosomal-dominant polycystic kidney disease (ADPKD) received octreotide for 12 months, and this was associated with a 6.3% reduction in liver volume, an 8% reduction in total kidney volume and stabilization of renal function. There was also a reduction of cyst size in fibrocystic disease of breast. These data suggest that the cyst fluid accumulation in different organs from patients with ADPKD is a dynamic process which can be reversed by octreotide. This is the first report of a case of simultaneous reduction in hepatic, renal and breast cystic volume with preservation of renal function in a patient with ADPKD receiving octreotide.

Low-dose rapamycin reduces kidney volume angiomyolipomas and prevents the loss of renal function in a patient with tuberous sclerosis complex.

Tuberous sclerosis complex (TSC) is caused by constitutively activated mammalian target of rapamycin (mTOR) resulting in non-malignant tumours of several organs including renal angiomyolipomas (AMLs). AMLs may originate renal failure, hypertension and spontaneous life-threatening bleeding. Recent reports suggest a possible beneficial role of the mTOR inhibitor rapamycin for TSC. However, safety and efficiency of rapamycin in TSC patients as an anti-proliferative agent are still undefined. A 40-year-old man with sporadic TSC and a history of spontaneous bleeding from his left kidney AMLs received low-dose rapamycin for 12 months, and this was associated with a reduction in bilateral kidney AML volume, stabilization and even improvement of renal function. There was also a reduction of facial angiofibromas, improvement of blood pressure control and absence of AML bleeding over this time period. Brain lesion images remained stable, and no significant rapamycin-associated side effects were noted. To the best of our knowledge, this is the first report of a case of reduction in renal AML volume together with preservation of renal function in a patient with TSC receiving low-dose rapamycin. These data suggest that it could be the result of the anti-angiogenic, anti-fibrotic and anti-proliferative effects of rapamycin.

Sacral radicular cysts in autosomal dominant polycystic kidney disease.

This is the first report of a case of sacral radicular cysts in a patient with autosomal dominant polycystic kidney disease (ADPKD). A 46-year-old woman with ADPKD was found to have bilateral sacral radicular cysts discovered incidentally by magnetic resonance imaging (MRI). Cysts arising from arachnoid or spinal meningeal sac should be considered one of the manifestations of a more widespread connective tissue disorder associated with ADPKD.