Search

Lithium intoxication is still an undefined and underestimated disease, especially those cases requiring extracorporeal treatment. Lithium is a monovalent cation with small molecular mass of 7 Da that has been regularly and successfully used since 1950 in the treatment of mania and bipolar disorders. However, its careless assumption can lead to a wide spectrum of cardiovascular, central nervous system and kidney diseases in case of acute, acute on chronic and chronic intoxications. In fact, lithium serum range is strict between 0.6 and 1.3 mmol/L, with a mild lithium toxicity observed at the steady-state of 1.5-2.5 mEq/L, moderate toxicity when lithium reaches 2.5-3.5 mEq/L, and severe intoxication with observed serum levels > 3.5 mEq/L. Its favorable biochemical profile allows the complete filtration and partial reabsorption in the kidney due to the similarity to sodium and also the complete removal by renal replacement therapy, that should be considered in specific poisoning conditions. In this narrative and updated review we discussed a clinical case of lithium intoxication, the different pattern of diseases attributable to excessive lithium load and the current indications for extracorporeal treatment., (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)

Diabetes and obesity are already recognized as potential risk factors for nephrolithiasis, especially for uric acid stones. Insulin resistance and hyperinsulinemia actively contribute to impaired ability to excrete an acid load and altered ammonium production, leading to a lower urinary pH compared to non-diabetic controls. All these electrolytic disorders play an important role in stone formation and aggregation, especially in uric acid stones. There are still missing points in scientific evidence if the increased risk in stone formation is already existing even in the prediabetic statuses (isolated impaired glucose tolerance, isolated impaired fasting glucose, and associated impaired glucose tolerance/impaired fasting glucose) as well as it is worth to consider the same level of risk. Urolithiasis is the most frequent urological cause of hospitalization in diabetic patients and its cost is usually higher compared to non-diabetic patients, but less is known in others altered glycaemic diseases. The aim of this review article is to focus on the association between stone formation and altered glycaemic statuses, beyond the already known link between nephrolithiasis and diabetes mellitus.

Introduction: Chronic renal failure (CRF) compromises nutrition, growth, puberty, glycometabolic homeostasis, and adipokine secretion (i.e. adiponectin, resistin, and leptin). Adipokines play a role in the clinical outcome, but data in paediatric patients is scant., Aim: To evaluate the link between kidney function, adiponectin, resistin, leptin, hormonal status, nutritional state and late outcome of CRF children., Materials and Methods: We studied leptin, adiponectin and resistin levels in 31 CRF patients (19 males, 12 females, aged 12.1 ± 4.47 years) managed conservatively, and 30 healthy age- and gender-matched controls. Clinical, auxological, biochemical, hormonal data, glucose and insulin levels were correlated with adipokine levels., Results: Six percent of patients had glycaemia T0' > 126 mg/dl, 23 % glycaemia T60' > 126, and 23 % glycaemia T120' ≥ 140. Glycated haemoglobin (HbA1c) measured during follow-up was in the normal range in all patients (4-5.6 %). Insulinaemia was significantly higher in CRF patients than controls. Homeostatic model of assessment-insulin resistance (HOMA-IR) levels were more elevated in patients (32 % had HOMA-IR > 2.5) than controls. Leptin levels were significantly higher in CRF patients than controls and differed significantly between males and females. Leptin correlated significantly with creatinine, body mass index (BMI), BA, pubertal stage, insulin-like growth factor 1, and HOMA-IR in females. Adiponectin levels were significantly higher in patients than controls, higher in patients with BMI < 85th centile and significantly inversely correlated to BMI, BA, haemoglobin, ferritin, proteins, albumin, and creatininuria. Resistin levels showed a direct correlation with C-reactive protein and an inverse correlation with haemoglobin., Conclusion: Normal resistin levels are an expression of both adequate nutritional state and controlled inflammatory state. Adiponectin could protect against chronic inflammation, atherosclerosis, and cardiovascular diseases. Preventing obesity and ensuring a correct nutritional state are primary goals for physicians following children with CRF. Adipokines could be a useful marker in the follow-up.

Background: Hyperphosphatemia is one of the main factors in the pathogenesis of secondary hyperparathyroidism. In addition, in dialysis patients elevated levels of phosphate and calcium times phosphate (Ca x P) ion product are associated with extraskeletal calcifications, as well as an increased risk of death. Cardiovascular calcifications may possibly be related to the high cardiovascular mortality seen in dialysis patients. In the USA the prevalence of hyperphosphatemia among dialysis patients is very high, over 60% of patients having serum P levels > 5.5 mg/dl, but no data are available for the Italian population, which follows different diet and dialysis schedules., Methods: We looked at a random sample of 638 patients enrolled in 29 outpatient dialysis units in Southern Italy (Campania and Sicily). Data were centrally analyzed after extraction from a computerized database. In each patient the average of two or more values obtained in the six-month observation period (from Jan. 99 to June 99) was calculated. Mean age was 61.2 years (95% CI 59.9-62.5) years, dialytic age 72.2 months (95% CI 67.4-77.0)., Results: Mean +/- SD (95% CI) levels of phosphate were 5.74 +/- 1.57 (5.62-5.86) mg/dl; total calcium 9.06 +/- 0.98 (8.98-9.14) mg/dl; Ca x P 51.4 +/- 14.4 (50.3-52.5) mg2/dl2; alkaline phosphatase was 167 +/- 119 (157-177) IU/L; intact parathyroid hormone (PTH) levels, available in a subset of 239 patients, were 318 +/- 413 (265-370) pg/ml. Among these patients 51.6% had serum P > 5.5 mg/dl, 36% > 6 mg/dl; Ca x P levels were > 55 mg2/dl2 in 35.5% of the population, 24% > 60 mg2/dl2; iPTH levels were < 100 pg/ml in 43%; 25.4% had hyperparathyroidism (defined as iPTH > 400 pg/ml), and only 19.5% of patients had PTH in the desired interval of 100 to 250 pg/ml., Conclusions: Compared to data reported from the USA, mean levels of phosphate, Ca x P, and PTH seem better controlled in this Italian hemodialysis population. However, in a significant number of patients these parameters were still outside the normal range. Both over-suppression of PTH levels and hyperparathyroidism are present, although surprisingly the former was more frequent. Treatment of hyperphosphatemia should be more aggressive in hemodialysis patients; PTH levels are difficult to maintain in the desired range of 100-250 pg/ml.

Complete deficiency of the complement C4A isotype is a known genetic risk factor for systemic lupus erythematosus (SLE). The disease phenotype of C4A-deficient patients has never been defined. Among 200 patients with SLE from five centers, 18 (9%) with C4A deficiency were identified. These individuals were compared to those who were C4A replete with regard to a series of clinical and serologic features. The only significant differences between the two groups were in the presence of renal disease (C4A deficient, 11%; C4A replete, 46%; P < 0.006) and a decrease in the serum concentrations of C3 (C4A deficient, 11%; C4A replete, 35%; P < 0.04). There was also a trend for the C4A-deficient individuals to have milder disease. In light of the tendency for C4A-deficient individuals to have lower serum concentrations of C4, it is important that such patients not be subjected to overly aggressive efforts to "normalize" their C4 levels.

Three of four children in a family have homozygous (less than 1% of normal) deficiency of factor H of the complement system and both parents, who are first cousins, are heterozygous for the same defect. The father and two of the H-deficient siblings also have a partial C2 deficiency. One of the children with combined deficiencies is affected by systemic lupus erythematosus with nephritis. No increased susceptibility to infections has been observed in the family. H deficiency is inherited in an autosomal codominant manner and is independently transmitted from C2 deficiency and HLA haplotypes. In the homozygous state it is associated with very low serum concentrations of B and C3, barely demonstrable as activated molecules. C5 is greatly reduced (less than 5%). Also, properdin and C6-9 are decreased. The findings in this family demonstrate that the occurrence of systemic lupus erythematosus in one of the children affected by a combined deficiency of factor H and C2 raises the question whether this pathology is related to the complete factor H or to the heterozygous C2 deficiency. Complete H deficiency is not necessarily accompanied by overt illness.