Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise.

BACKGROUND AND AIMS: Urinary neutrophil gelatinase associated lipocalin (uNGAL) and urinary kidney injury molecule-1 (uKIM-1) are markers of acute kidney injury. The albuminuria is a well-known abnormality after physical exercise. The aim of this study was to investigate changes in uNGAL and uKIM-1 after intensive exercise causing albuminuria. METHODS: The study population consisted of 19 participants (10 males and 9 females). The mean age of participants was 35.74 years. All were fit amateur runners; the mean body mass index was 21.99 in females and 24.71 in males. The subjects underwent a graded treadmill exercise test (GXT) according to the Bruce protocol. Maximal oxygen consumption (VO2max) was measured. Immediately before and after the test urine was collected. Urinary creatinine, albumin, NGAL, and KIM-1 were measured. Albumin to creatinine (ACR), KIM-1 to creatinine (KCR), and NGAL to creatinine (NCR) ratios were calculated. RESULTS: The mean VO2max was 53.68 in females and 59.54 mL/min/kg in males. Albuminuria and ACR were significantly higher after exercise. An increase in the ACR from 8.82 to 114.35 mg/g (p < 0.01) was observed. uKIM-1 increased significantly after exercise from 849.02 to 1,243.26 pg/mL (p < 0.05). KCR increased from 1,239.1 to 1,725.9 ng/g but without statistical significance (p = 0.07). There were no statistical changes in pre- and post-run uNGAL levels. There was no correlation between post-GXT albuminuria and uKIM-1. CONCLUSIONS: uKIM-1 is a very sensitive marker of kidney dysfunction. In our study, uKIM-1 increased significantly after a very short period of exercise. It is not clear if the increase in KIM-1 is caused by post-exercise albuminuria.

A case report of Gitelman syndrome resulting from two novel mutations in SLC12A3 gene / El caso del síndrome de Gitelman causado por dos nuevas mutaciones en el gen SLC12A3

Introduction: Hypokalaemia is a common clinical problem. A potential but commonly overlooked cause of hypokalaemia is Gitelman syndrome. Material and methods: A 26-year-old man was admitted to the hospital due to syncope with general and muscular weakness and muscle cramps. The patient's history revealed previous recurrent syncope events associated to hypokalaemia with the lowest serum potassium value being 2.6mmol/l. At admission, blood pressure was normal and no changes were found at physical examination. Laboratory tests showed mild hypokalaemia (3.0mmol/l), hypomagnesaemia (1.36mg/dl), hypocalciuria (< 40mg/24h), and metabolic alkalosis (HCO3− 29.7mmol/l, BE 5.3mmol/l). Results: Further laboratory tests (FeK, TTKG) confirmed inappropriate kaliuresis. Conn's disease was excluded by hormonal and imaging assessments. Genetic testing was performed and two novel heterozygous mutations: c.35_36insA and c.1095+5G>A were found in transcriptNM_000339.2 in SLC12A3 gene. Conclusion: The patient was diagnosed with Gitelman syndrome and was treated with supplements of potassium and magnesium (AU)

Introducción: La hipopotasemia es un problema clínico común. El síndrome de Gitelman es una posible causa de hipopotasemia a veces no reconocida. Material y métodos: Un hombre de 26 años de edad ingresa en un hospital por causa de un síncope, debilidad generalizada y calambres musculares. La historia clínica del paciente reveló la incidencia del síncope con hipopotasemia recurrente con el valor más bajo de potasio en 2,6mmol/l. En el ingreso, el paciente presentaba una presión arterial normal y la exploración física no reveló ninguna enfermedad. La evaluación del laboratorio demostró una hipopotasemia leve (K+ 3,0mmol/l), hipomagnesemia (Mg 1,36mg/dl), hipocalciuria (<40mg/24h) y alcalosis metabólica (HCO3- 29,7mmol/l, exceso de base 5,3mmol/l). Resultados: Otras pruebas de laboratorio (FeK, TTKG) confirman una caliuresis inadecuada. La enfermedad de Conn fue excluida tras la evaluación hormonal y radiológica. Se realizaron las pruebas genéticas y 2 mutaciones heterocigóticas: c.35_36insA y c.1095+5G>A fueron encontradas en la transcripción NM_000339.2 del gen SLC12A3. Conclusión: El paciente fue diagnosticado con el síndrome de Gitelman y fue tratado con suplementos de potasio y magnesio (AU)

A case report of Gitelman syndrome resulting from two novel mutations in SLC12A3 gene.

INTRODUCTION: Hypokalaemia is a common clinical problem. A potential but commonly overlooked cause of hypokalaemia is Gitelman syndrome. MATERIAL AND METHODS: A 26-year-old man was admitted to the hospital due to syncope with general and muscular weakness and muscle cramps. The patient's history revealed previous recurrent syncope events associated to hypokalaemia with the lowest serum potassium value being 2.6mmol/l. At admission, blood pressure was normal and no changes were found at physical examination. Laboratory tests showed mild hypokalaemia (3.0mmol/l), hypomagnesaemia (1.36mg/dl), hypocalciuria (< 40mg/24h), and metabolic alkalosis (HCO3(-) 29.7mmol/l, BE 5.3mmol/l). RESULTS: Further laboratory tests (FeK, TTKG) confirmed inappropriate kaliuresis. Conn's disease was excluded by hormonal and imaging assessments. Genetic testing was performed and two novel heterozygous mutations: c.35_36insA and c.1095+5G>A were found in transcript NM_000339.2 in SLC12A3 gene. CONCLUSION: The patient was diagnosed with Gitelman syndrome and was treated with supplements of potassium and magnesium.

Posttransplant encapsulating peritoneal sclerosis: presentation of cases and review of the literature.

BACKGROUND: Encapsulating peritoneal sclerosis (EPS) is a rare but serious complication of peritoneal dialysis (PD). EPS almost exclusively occurs in patients treated longer than 3-5 years on PD. The more severe clinical features of EPS may develop if PD is discontinued (patient transferred to hemodialysis or transplanted). METHODS: All PD patients diagnosed with EPS after transplantation were identified, and their data were compared with those of non-EPS PD patients transplanted in our unit between 1994 and 2010. RESULTS: Four EPS cases were diagnosed among 157 transplanted PD patients. Mean renal replacement therapy and PD-only duration were 103.8 and 83.5 months in EPS and 26.5 and 22.2 months in non-EPS patients, respectively. All EPS patients (n = 4) required high-volume dialysis, 2 received icodextrin, 3 were high transporters, 1 had recurrent intraperitoneal bleeding, 4 received beta-blockers and 3 had peritonitis incidents. All required surgical intervention within 1-3 months after kidney transplantation (KT). Diagnosis of EPS was based on clinical symptoms, surgery, radiologic and histopathology findings. Treatment consisted of adhesiolysis (all), parenteral nutrition (PN) (3/4) and tamoxifen (all). One patient died 49 months after EPS diagnosis. CONCLUSIONS: First, bowel obstruction symptoms in long-term PD patients undergoing KT may suggest EPS. Second, long-term PD patients showing features of technique failure are at high risk of EPS after KT. Third, adhesiolysis, PN and tamoxifen are the available treatment options in EPS patients post KT. And finally, referral of eligible patients to a transplant waiting list early after starting PD may contribute significantly to EPS prevention in clinical practice.