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Zinc is an essential micronutrient for the organism and is critical for the functional and structural integrity of cells. Determination of the amount of trace element concentrations in tissues such as hair samples have been used for the evaluation of the metabolic status especially in children. Unlike serum zinc, concentrations of zinc in hair are more stable and indicative of variations over time. The purpose of this study is to assess the zinc status of healthy school-age children in Kayseri (Turkey) by measuring the zinc level in hair samples and its association with BMI and the frequency of intake of zinc-rich foods. A total of 527 healthy children, including preadolescent (n = 360) aged 6-10 years and adolescent (n = 167) aged 11-15 years were included in this study. Hair samples were analyzed for zinc content by the inductively coupled plasma-mass spectrophotometry. Analysis of 527 healthy children showed that the mean hair zinc level was 186 ± 77 μg/g. Mean hair zinc level was lower in preadolescent age group than adolescents. There was no significant relationship between the monthly income of the family and the zinc-rich food intake and the zinc level of the hair. Our study shows that samples for analysis of zinc can be obtained with a noninvasive method for determining cases of deficiency during periods of rapid growth. However, further studies are needed to determine the normal tissue zinc level in healthy children, especially in our country and including different geographical regions.

Renal involvement in non-Hodgkin lymphoma is a recognized development, but it mostly follows a diagnosis of lymphoma. We describe a rare case of a T-cell-type non-Hodgkin lymphoma that first presents as nephromegaly in a 5-year-old girl admitted to the emergency department with abdominal pain. Further investigation revealed bilateral nephromegaly, but the results of blood tests, imaging studies, and bone marrow aspiration were inconclusive. During the second week of hospitalization, significant physical examination revealed an enlarged lymph node in the anterior cervical chains, confirming a diagnosis of Non-Hodgkin's lymphoma. This case illustrates that it is important to have a high degree of suspicion in any patient presenting with unexplained enlarged kidneys without any identifiable cause because it could be the first presentation of a hematologic malignancy.

Detection of a cystic lesion in the liver suggests simple cysts, multiple cysts arising in the setting of polycystic liver disease (PCLD), parasitic or hydatid (echinococcal) cysts, cystic tumors, and abscesses. These conditions can usually be distinguished on the basis of the patient’s symptoms and the radiographic appearance of the lesion [1]. The presence of constitutional symptoms, such as pallor, anorexia, fever or weight loss, may point toward a malignant lesion or infection, but our patient had no medical history or signs of these upon physical examination. Ultrasound of his abdomen revealed a huge liver cyst of 90 mm occupying almost the whole left lobe with mild internal echoes all suggestive of hydatid cyst. The kidneys, spleen and pancreas appeared normal. Abdominal computed tomography (CT) was used to delineate the cystic lesion within the liver. Indeed, the CT confirmed a huge, thick-walled cyst of 90 mm in diameter, occupying the left lobe of the liver in segment I. Hydatid disease (HD), or echinococcosis, is a zoonotic infection caused by the larval stages of the cestodes belonging to the genus Echinococcus. Cystic echinococcosis (CE) is the most common form of HD, and occurs as the result of infection by the larval stages of E. granulosus, which has a worldwide distribution and continues to be a major health problem in developing countries [2–4]. Oncosphere larvae hatch in the duodenum and are carried to the liver through blood vessels or lymphatics. About 65 % are trapped in the liver (first filter), which is the most commonly involved organ (52–77 % of cases); the remaining 25 % are trapped in the lungs (second filter) and less than 10 % reach various organs through the systemic circulation [5]. The symptoms of liver hydatid cysts differ depending on the size and number of cysts, but also on the mass effect within the liver and upon surrounding structures. Patients are usually asymptomatic, but may present with right/epigastric pain, nausea, and vomiting [1]. Considering that the early stages of infection are usually asymptomatic, the diagnosis of hydatid cyst depends on clinical suspicion. Diagnosis is made by history of exposure, by radiological and ultrasound cyst detection, and by serology [6]. The diagnosis of hydatid disease in our patient was confirmed by a strongly positive serum ELISA and indirect hemagglutination test (IHA) for Echinococcus. Treatment This article refers to the article that can be found at http://dx.doi.org/ 10.1007/s00467-012-2282-x.

Our patient initially presented with lupus nephritis and hyperkalaemia, with a normal anion gap and hyperchloraemic metabolic acidosis. A wide range of conditions have to be taken into account in the differential diagnosis for hyperkalaemia. Based on our patient’s laboratory findings, acute renal failure, drugs, blood transfusion and hemolysis were ruled out. Persistent hyperkalaemia and normal anion gap metabolic acidosis led us to suspect the presence of Type 4 RTA. This is included in the general classification of RTA as its cardinal feature is hyperkalaemia with a mild (normal anion gap) metabolic acidosis and normal measured urinary acidification [1]. Unlike distal RTA, in which proton secretion is defective, causing high urine pH, the main defect in Type 4 RTA is transport abnormality of the distal tubule, which is secondary to aldosterone deficiency, resistance or inhibition. The primary effect of aldosterone on the collecting duct is to stimulate sodium reabsorption and potassium secretion in principle cells, which results in an increase in the negative electrical potential of the lumen, promoting proton secretion. Aldosterone also directly affects the alpha intercalated cells to promote proton secretion by upregulating the expression of the proton ATPase as well as carbonic anhydrase. Thus, patients that are aldosterone deficient or resistant to aldosterone have increased sodium excretion [1, 2]. Our patient also had mildly increased of sodium excretion. The preferred method to estimate potassium excretion by the distal tubule is the TTKG. Our patient’s TTKGwas 5 in the presence of hyperkalaemia (normal >10), which indicates a defect in potassium secretion. A low TTKG is associated with aldosterone deficiency or resistance. The renin activity was 2.3 (5–27.8) pg/mL and the aldosterone level was 10 (13–340) pg/ L in the presence of high plasma levels of potassium. She appeared to have two distinct disorders, namely, renin– aldosterone deficiency or hyperkalaemic distal RTA. Her urine pH was 5.5 when the blood pH was 7.3, and the HCO was 16.8 mEq/L, which are suggestive of hyporeninaemic hypoaldosteronism (Type 4 RTA). Type IV RTA is the most common form of renal tubular acidosis and occurs in various disorders (Table 1). The most common causes of HH include diabetic nephropathy, tubulointerstitial disease and, in particular, interstitial nephritis associated with non-steroidal anti-inflammatory drugs (NSAIDs). Other causes in which hypoaldosteronism is present but not matched by hyporeninism include adrenal destruction (whether surgical, malignant or hemorrhagic), This article refers to the article that can be found at doi:10.1007/ s00467-2011-2040-5