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Addison disease is due to the destruction or dysfunction of the entire adrenal cortex. Nowadays, the causes of adrenal insufficiency are autoimmune disease for 70-90% and tuberculosis for 7-20%. Many typical signs and symptoms, such as hyponatremia, hyperkalaemia, or renal insufficiency can represent the reasons for a nephrology consultation, especially in conditions of urgency, and they can easily be confused with other causes. Moreover, the fact that in a short time range we have diagnosed the three cases described as a guide in this review, has aroused our attention as nephrologists on a disease in which we have probably already encountered but without recognizing it. The blood tests showed in all three patients severe electrolyte disorders and acute renal failure which will be discussed in their physiopathogenetic mechanisms. In a peculiar way, these alterations were not controlled with repolarizing solutions, fluid replacement and increased volemia, but only after steroid administration. In conclusion, in this review all the known pathogenic mechanisms causing disorders of nephrological interest in adrenal insufficiency are discussed.

Background and Aims Spectrum of acute severe respiratory syndrome Coronavirus 2 (SARS-CoV-2) ranges from mild to critical and probably mortality rate is largely underestimated. Complications may represent different manifestation of a profound endothelial dysfunction and injury. Biopsies reveal macro and microvascular thrombosis involving larger and smaller vessels. Different Authors described accumulation of inflammatory cells across vascular bed, viral inclusions and apoptotic bodies across vascular bed. Endotheliitis leads to loss of vessel integrity with bleedings and lumen restriction with tissue ischemia and necrosis. SARS-CoV-2 also can cause vasculitis and a systemic inflammatory vascular disease with COVID-19-associated coagulopathy. Several cases of vasculitis have been described during COVID-19 pandemy but in literature, to our knowledge, there are few cases of patients developing vasculitis after SARS-CoV-2 infection. Method A 59-year-old male patient in chronic haemodialysis with hypertension, chronic thrombocytopenia, uncertain history of type 2 diabetes mellitus and recent COVID-19 pneumonia (1 month before) was admitted to our E.R. with psycho-motor slowdown, dyspnoea, profound hypotension, diffuse and extensive purpura especially on extremities and nose with petechiae and ecchymoses, thrombocytopenia, widespread arthritis and myalgia and atrial fibrillation with high ventricular response. Laboratory tests revealed leucocytosis with elevation of inflammatory markers (GB 15.6 x 103/µL CRP 6.61 mg/dl, procalcitonin 2.64 ng/ml), thrombocytopenia (PLTs 55 x 103/µL), Hb 11.2 g/dl, increased amylase (444 UI/L) and lipase (608 UI/L), hyperkaliaemic metabolic acidosis, mild impaired blood clotting with normal fibrinogen and severe D-Dimer elevation (3453 mcg/ml), normal haptoglobin and bilirubin. SARS-CoV-2 rapid antigen test and three molecular swab tests (at admission and during recovery) were negative. Contrast-enhanced chest-abdomen CT did not demonstrate relevant findings. Results We suspected thrombotic thrombocytopenic purpura, COVID-19 related vasculitis or an autoimmune disease reactivation after SARS-CoV-2 or other concurrent viral infections. A peripheral blood smear excluded presence of schistocytes, HBV, HCV, HIV, c-ANCA, p-ANCA, LAC anti-mitochondrial and ENA antibodies were negative, such as complement factor C4 (C3 at low limits). IgA immunoglobulins resulted increased (952 mg/dl). We administered intravenous (IV) hydration, analgesic therapy, broad spectrum antibiotics and Methylprednisolone 40 mg IV without benefit. Three days after clinical conditions were critical with further neurological deterioration and haemodynamic instability, consequently we started methylprednisolone 1 g/day IV for three days, followed by oral prednisone 25 mg/die with rapid improvement of clinical conditions and laboratory findings. A skin biopsy revealed a variable and discontinuous presence of C4d and IgM along capillary walls and traces of IgG, supporting the hypothesis of an immune-mediated vasculitic process. Patient was discharged in stable condition with Prednisone 25 mg/die per os. Later we learned that patient had been hospitalized again for severe anaemia, thrombocytopenia and septic shock with fatal outcome. Conclusion SARS-CoV-2 clinical spectrum appears to be extremely varied; the direct cytolysis and the immune-mediated damage are among the most accredited hypotheses on disease physiopathology, but molecular mimicry mechanisms may also be involved. Vascular endothelium can be considered among the first targets. Vasculitis are frequently described in literature during COVID, this case, instead, is an anecdotal report of severe angiitis arising after swab negativization, underlying the possibility that hyperinflammation can either cause an autoimmune syndrome de novo or trigger a flare-up of a pre-existing condition.

Background and Aims Osteoporosis in hemodialysed (HD) patients with Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD) is a debilitating clinical condition with complex therapeutic management. In fact, most of the drugs commonly used to counteract osteoporosis are generally contraindicated when Glomerular Filtration Rate (GFR) is lower than 30 ml/min. Denosumab (DMab) is a monoclonal antibody approved for the treatment of osteoporosis and does not require dose adjustment in case of impaired renal function. For this reason, since 2014 this drug has been used by nephrologists for the treatment of osteoporotic patients also in hemodialysis. Although the interest and diffusion in this specialized clinical field are growing, only few data are still available in literature. The aim of the study was to evaluate the efficacy and safety of denosumab in long-term therapies in hemodialysed patients. Method Since November 2013, a total of 19 hemodialysed patients have been treated with denosumab annually (4) or semi-annually (15) for up to 48 consecutive months. During the course of therapy, the laboratory parameters of osteo-mineral metabolism were monitored, and Qualitative UltraSonography (QUS) or Computerized Bone Mineralometry (CBM) were used alternatively, every 30 months and every 2 years, respectively (depending on guidelines recommendation for both radiological methods and timing). Results 7/19 patients completed at least 30 months of follow-up, observing a substantial stability of blood calcium and phosphorus values, against a reduction in the mean values of B-CrossLaps and ostase (respectively from 2975.32 to 1852.25 pg/ml and from 28.13 to 11.93 mcg/L). Comparison of QUS exams demonstrated improved T-score (-4.71 to -4.17) and reduced fracture risk (13% to 8%). The results of the CBMs confirmed the stability of the bone disease at the spine and the improvement of the Tscore at the femoral level (from -3.5 to -3). It should be noted that in our samples two patients achieved the longest observation period (48-month follow-up in continuous therapy), in which the stability of bone damage was observed at CBM compared to the start of treatment. Only one fracture has been recorded. Conclusion We underline that close biochemistry monitoring and careful evaluation of the therapeutic procedures before and after DMab administration helped us to minimise and promptly correct adverse effects due to hypocalcemia. In addition we are particularly satisfied to report in most patients a significant reduction of pain and an improvement of mobility. The results collected are consistent with acceptable safety and demonstrated efficacy of denosumab in hemodialysis patients.

Background and Aims COVID-19 has heterogeneous clinical manifestations. SARS-CoV-2 related AKI and hypercoagulability are negative prognostic factors. The incidence of thromboembolic events is about 30%, of AKI up to 20%. We report a patient with severe AKI who required hemodialysis (HD) and developed a massive DVT developing from the femoral CVC, and belatedly testing positive for SARS-CoV-2 in the absence of typical pulmonary involvement. Method A 53-year-old male with a clinical history of hypertension, type II diabetes mellitus, in therapy with metformin and ace-inhibitor, was admitted to our E.R. with diarrhea, nausea and vomiting for about 2 days. Main signs: ideomotor slowdown, mild hypohydration and reduced urine output (unrelevant sediment). Initial blood tests showed severe AKI with hyperkalemic metabolic acidosis and hyponatremia (sCreatinine 18.76 mg/dl, BUN 161 mg/dl, K+ 7.8 mmol/l, Na+ 128 mmol/L, HCO3- 9.8 mmol/l). Mild neutrophilic leukocytosis with lymphopenia was detected, with slightly increased inflammation indices (CRP 1.05 mg / dl, D-dimer 720 ng / ml). CT scan: absence of typical SARS-CoV-2 signs, normal kidneys, no dilation of urinary tract. SARS-CoV-2 rapid antigen test and the first molecular swab test were negative. After femoral CVC insertion, HD was needed for a few sessions. Broad range antibiotic therapy was also set. On Day 3: a second SARS-CoV-2 PCR swab test resulted negative. He never manifested fever or dyspnea. On Day 6, despite an improvement of renal function (sCr 2.7 mg/dl), the patient, although he walked, presented right leg pain with signs of DVT. Ultrasound and angio-CT scan documented peri-catheter DVT extended to the common femoral and external iliac vein and superficial femoral vein involvement, without pulmonary embolism. I.v. therapy with sodium heparin was therefore started with quite a difficulty in reaching the expected range. On day 8, massive flittene appeared, the CVC was removed and a caval filter was placed; marked neutrophilic leucocytosis and increased inflammatory indices (CRP 11.50 mg/dl) was documented. Nevertheless, thrombosis has progressed to the entire venous axis and the inferior cava. Through a tibial vein introducer local i.v. alteplase was also started. Just after, copious bleeding from the site of the removed CVC followed by haemorrhagic shock occurred and the patient was transferred to the ICU (D-dimer 219800 ng/ml). The same day a third swab for SARS-CoV-2 resulted positive while a further CT-scan did not show signs of virus-like interstitial pneumonia. On the following day (day 9) the patient underwent thrombus aspiration (Aspirex®S device) and fasciotomy of the right leg for a compartment syndrome. Results Despite the continuation of heparin, PTT ratio was never >1.5, with an extension of DVT and also involvement of the contralateral iliac vein, as well as a worsening of the clinical-laboratory picture and patient’s death on day 14. Serum complement, autoantibodies (ANA, ANCA, ENA, ANTI-dsDNA, anti-cardiolipin, AMA, anti-B-glycoprotein) and factor V Leiden test were normal. All blood cultures were found to be sterile. Conclusion Our case confirms the heterogenicity of COVID-19 manifestations, often without pulmonary involvement. According to our experience from the onset of the pandemic, SARS-CoV-2 can also be found later in patients with already advanced organ damage. In this case, in the absence of other possible factors, AKI and intestinal involvement may have been early signs of COVID-19, with a virus initially not detectable in the nasopharyngeal mucosa. Furthermore, the increased thromboembolic risk of COVID-19 should not be underestimated in the presence of risk factors as external devices, also given the difficult management of anticoagulation target. Anticoagulant prophylaxis in cases with doubtful symptomatology and CVC must be considered even in non-bedridden patients, due to the current risk of SARS-CoV-2 infection.

Background and Aims The bidirectional relationship between renal disease and malignancy is well known and requires specialized approaches. For this reason, onconephrology has emerged as a new evolving field in the last few years. Method In a dedicated nephrology clinic, we followed 54 metastatic cancer patients (pts) (23 F, 31 M; mean age 68.3 ± 9.8 yrs) during target therapy (TT). They were in treatment for different types of cancer (kidney n=32, colo-rectal n 6=, breast n=5, lung n=5, neuroendocrine n=2 and other n=4). 12 pts were taking anti-VEGF (group 1), 26 pts tyrosine kinase inhib (group 2), 7 pts mTOR inhb (group 3) and 9 pts immune-checkpoint (group 4). Kidney biopsies were not performed because of increased risk or for improvement of RI when changes in TT were performed. Renal injury (RI) occurred on average after 8.9 months from the start of TT. We compared the effects of the different therapeutic interventions on changes of renal function between T0 (before TT) and T1 (during TT). We also documented changes in oncologic therapeutic prescription due to renal injury and their effects at T2 (follow up). Kidney biopsies were not performed because of increased risk or for improvement of RI when changes in TT were performed. A two way repeated measures ANOVA (group x time) was used to compare the effects of the four groups on serum creatinine (sCr), creatinine clearance and proteinuria 24 h (PU) at T0 and T1. Results Mean basal sCr of pts taking antiVEGF was 0.95 mg/dl, eGFR (MDRD) 81.9 ml/min and PU 196 mg 24h. At T1 (8.37 months on average) sCr was 1.74 mg/dl, eGFR 62 ml/min and PU 1777 mg 24h. Mean basal sCr of pts taking tyrosine kinase inhib was 1.24 mg/dl, eGFR 55 ml/min and PU 145 mg 24h. At T1 (13 months on average) sCr was 1.59 mg/dl, eGFR 46 ml/min, and PU 916 mg 24h. Mean basal sCr of pts taking mTOR inhib was 1.28 mg/dl, eGFR 57 ml/min and PU 150 mg 24 h. At T1 (6.3 months on average) sCr was 2.1 mg/dl, eGFR 31.7 ml/min and Pu 345 mg 24 h. Mean basal sCr of pts taking immune-checkpoint was 1.27 mg/dl, eGFR 59 ml/min and PU 150 mg 24h. At T1 (months on average) sCr was 3.74 mg/dl, eGFR 30 ml/min and PU 257 mg 24h. A significant increase in sCr was observed when comparing T0 and T1 among the four groups but only a statistical trend (P = 0.088) was found for the group by time interaction thus not allowing us to speculate on potential differences between the different pharmacological interventions. Lower Creatinine clearance and higher PU, were found at T1 in pts on anti-VEGF compared to those on immune-checkpoint inhibitors. We generally observed an improvement of renal function after reduction of TT dose or its temporary discontinuation (27.8%), but definitive interruption was required in 31.8% of cases. In 2 diabetics pts on tyrosine kinase inhib we observed persistent nephrotic proteinuria and progressive worsening of renal function and beginning of chronic hemodialysis neverthless discontinuation. At the end of follow-up 5 pts reached end-stage renal disease (1 pt was taking antiVEGF, 2 pts tyrosine kinase inhib, 2 immune-checkpoint) and 6 pts were dead (4 pts were taking antiVEGF and 2 pts tyrosin kinasi inhib). Conclusion Our findings suggest that careful monitoring of renal function is needed to optimize the use of TT, also considering that RI can be multifactorial. Onconephrologists work with the aim of trying to ensure the continuity of anti-tumoral therapy, knowing how far they can go to maintain a balance between kidney function (even sacrificing part of it) and patient survival. In conclusion, nephrologists should be increasingly familiar with the diagnosis, management and treatment of renal diseases and the complexity of this field may benefit from well-defined multidisciplinary management by a dedicated team

Clinical Background: Cancer therapeutics (for both solid and hematological malignancies) have evolved over the last two decades, from traditional chemotherapies to novel treatments. A better supportive care, older patients with comorbidities who receive multiple chemotherapeutic and pharmacological regimens, multiple CT scans with contrast agents, and new therapeutic options are also increasing the number of cancer patients who can develop acute kidney injury (AKI) or chronic kidney disease (CKD). Challenges: Targeted therapies and immunotherapies, which harness the body's own immune system to fight cancer cells have led to improved survival in cancer patients, yet all are associated with many organ toxicities. Renal toxicity is mainly represented by acute tubular-interstitial damage, glomerular lesions, thrombotic microangiopathy, tumor lysis, proteinuria, arterial hypertension, AKI, CKD, and secondary fluid/electrolyte disturbances. On the other hand, it is important to consider how the presence of CKD, AKI, and other renal disorders may affect treatment options for the oncologists and patient's outcome. All these features require a specialized approach. Prevention and Treatment: A new evolving field, namely Onconephrology, has emerged during the last few years, including the broad spectrum of renal disorders that can arise in patients with cancer. Nephrologists have become an indispensable part of the multidisciplinary cancer care teams, but a clear and updated knowledge of solid and hematological malignancies, always new anticancer therapies, and their relationships with kidney function is essential to ensure the highest quality of care. In this chapter, we summarize the principal aspects of this new field of Nephrology.

Clinical Background: Cancer therapeutics (for both solid and hematological malignancies) have evolved over the last two decades, from traditional chemotherapies to novel treatments. A better supportive care, older patients with comorbidities who receive multiple chemotherapeutic and pharmacological regimens, multiple CT scans with contrast agents, and new therapeutic options are also increasing the number of cancer patients who can develop acute kidney injury (AKI) or chronic kidney disease (CKD). Challenges: Targeted therapies and immunotherapies, which harness the body's own immune system to fight cancer cells have led to improved survival in cancer patients, yet all are associated with many organ toxicities. Renal toxicity is mainly represented by acute tubular-interstitial damage, glomerular lesions, thrombotic microangiopathy, tumor lysis, proteinuria, arterial hypertension, AKI, CKD, and secondary fluid/electrolyte disturbances. On the other hand, it is important to consider how the presence of CKD, AKI, and other renal disorders may affect treatment options for the oncologists and patient's outcome. All these features require a specialized approach. Prevention and Treatment: A new evolving field, namely Onconephrology, has emerged during the last few years, including the broad spectrum of renal disorders that can arise in patients with cancer. Nephrologists have become an indispensable part of the multidisciplinary cancer care teams, but a clear and updated knowledge of solid and hematological malignancies, always new anticancer therapies, and their relationships with kidney function is essential to ensure the highest quality of care. In this chapter, we summarize the principal aspects of this new field of Nephrology.

Background/Aims: Multiple myeloma (MM) represents 10% of all haematologic malignancies. Renal involvement occurs in 50% of MM patients; of them, 12-20% have acute kidney injury (AKI), with 10% needing dialysis at presentation. While hemodialysis (HD) has no effect upon circulating and tissue levels of monoclonal proteins, novel apheretic techniques aim at removing the paraproteins responsible for glomerular/tubular deposition disease. High cut-off HD (HCO-HD) combined with chemotherapy affords a sustained reduction of serum free light chains (FLC) levels. One alternative technology is haemodiafiltration with ultrafiltrate regeneration by adsorption on resin (HFR–SUPRA), employing a “super high-flux” membrane (polyphenylene S-HF, with a nominal cut-off of 42 kD). Aim of our pilot study was to analyze the effectiveness of HFR-SUPRA in reducing the burden of FLC, while minimizing albumin loss and hastening recovery of renal function in 6 subjects with MM complicated by AKI. Methods: Six HD-dependent patients with MM were treated with 5 consecutive sessions of HFR-SUPRA on a Bellco® monitor, while simultaneously initiating chemotherapy. Levels of albumin and FLC were assessed, calculating the rates of reduction. Renal outcome, HD withdrawal and clinical follow-up or death were recorded. Results: All patients showed a significant reduction of FLC, whereas serum albumin concentration remained unchanged. In three, HD was withdrawn, switching to a chemotherapy alone regimen. The other patients remained HD-dependent and died shortly thereafter for cardiovascular complications. Conclusion: Our study suggests that HFR-SUPRA provides a rapid and effective reduction in serum FLC in patients with MM and AKI, while minimizing the loss of albumin. When started early in combination with chemotherapy, blood purification by HFR-SUPRA was followed by the recovery of renal function in half of the patients treated.

Hemodialysis (HD) may induce vascular stiffness through several mechanisms. We sought to determine the role of dialysis vintage (DV) on the development of cardiovascular alterations. We studied 14 patients in chronic HD and 24 newly diagnosed never treated hypertensive patients and 16 normotensive controls. The patients in HD were divided in two groups according to DV: 60-months (DV>60,n=7). After HD session, when dry weight was reached, we evaluated peripheral blood pressure (pBP), the parameters derived by tonometric analysis of the pulse waveform (central blood pressure-cBP-, Subendocardial Viability Ratio-SEVR-, carotid-femoral pulse wave velocity-cf-PWV-) and those derived from echocardiography: ejection fraction (EF-for systolic function) and E/e’ (for diastolic function), and the ultrafiltration volume (UV). Calcium/phosphate (Ca/P) levels, serum albumin, and Kt/V were evaluated retrospectively on repeated measurements over the past 5 years. All the groups were similar for sex and BMI, both DV60 were older than hypertensives and controls (58.33±3.71 and 59.83±7.98 vs 44.14±1.28 and vs 40.63±2.05 years, respectively, P60 presented similar levels of Ca/P, serum albumin, Kt/V and UV. pBP was increased and similar to hypertensives in DV>60 vs DV60 vs DV60 vs DV60 vs DV In conclusion, only patients with DV>60 presented increased aortic stiffness. This was associated to higher BP and diastolic dysfunction. Hence, chronic HD, particularly after 60 months, may play a putative role in developing cardiovascular alterations in patients with end-stage renal disease.

In elderly subjects, renal insufficiency and osteoporosis often coexist with high risk of fracture and elevated socio-economic burden. Today a large number of effective anti-osteoporotic drugs are available but generally they are contraindicated in patients with chronic kidney disease (CKD) because of their progressive accumulation. Denosumab, instead, does not require dose adjustments for different degrees of renal impairment so it can be a valid treatment in osteoporotic patients with CKD. Limited data are available in the literature concerning the use of denosumab in hemodialysis (HD). The aim of our study was, therefore, to study the efficacy and tolerability of this drug in this particular subset of patients. We retrospectively reviewed the charts of 12 osteoporotic HD patients who received a single 60-mg subcutaneous dose of denosumab every 6 months for an observation period of 24 months. Serum electrolyte, markers of bone turnover and quantitative ultrasound (QUS) were evaluated. Over 24 months, we observed a gradual improvement of bone metabolism: β-CrossLaps from 2567.08 ± 1264 to 1492.5 ± 1182.5 pg/ml; bone alkaline phosphatase (BALP) from 33.5 ± 28.8 to 11.8 ± 3.7 mcg/l, and of QUS index (T-score from −5.33 ± 1.58 to −4.84 ± 1.2; risk of fracture from 13.9 ± 4.7 to 11.07 ± 5.3 %). Few cases of hypocalcemia were detected, more significant after the first and second injection, but with careful monitoring of serum calcium and rapid therapy adjustment we could easily manage serum Ca levels. Our pilot experience highlights the safety and efficacy of denosumab in the treatment of osteoporosis in HD patients, potentially supporting its use to reduce the burden of fractures in this patient population.

Idiopathic retroperitoneal fibrosis (IRF) is a rare disease characterized by fibro-inflammatory reaction surrounding ureters and other inner organs with possible secondary renal involvement. Symptoms are aspecific and recurrent phases of activity are generally associated with elevation of inflammatory indices. 18F-FDG-PET is nowadays an important tool for the detection of this disease, allowing differentiation between metabolically active tissue and fibrotic one. The purpose of this study was to investigate the role of 18F-FDG-PET in the management of IRF and to evaluate possible correlations between biochemical parameters and PET/CT findings of disease activity. We enrolled seven consecutive patients with IRF (in five histology proved the disease) observed from 2003 to 2012 (5 M:2 F, mean age 53.8 years, range 44-86 years). All patients presented with fever as first symptom; two had obstructive renal failure requiring hemodialysis; one underwent monolateral nephrectomy for parenchyma infiltration; six presented ureteral involvement; three underwent ureteral stent placement. For each patient, during a mean total follow-up of 26.5 months we evaluated serum creatinine, BUN, Hb, RBCs, WBCs, PLT, CRP, ESR. Periodic 18F-FDG-PET/CT scans (every 5.9 months-mean) were performed in all patients. Statistical evaluation was performed using "stepwise regression" analysis. Steroids and immunosuppressive agents induced a progressive normalization of PET/CT scans in all patients at the end of follow-up. Stepwise regression analysis showed that BUN, serum creatinine and CRP only if considered together, significantly correlated with SUV max (p value = 0.000003057). 18F-FDG-PET is a useful tool for clinical decision making in patient with IRF, allowing to evaluate the efficacy of the pharmacological treatment and to detect early recurrences, to modify the therapeutic approach. Acute phase reactants are not reliable alone for the management and the follow-up as they are often not concordant with metabolic assessment of the disease. In patients with ureteral involvement, CRP together with BUN and serum creatinine has a significant correlation with PET/CT results, and can help physicians in therapeutic approach, better than a single parameter.

A renal biopsy in a case of systemic lupus erythematosus (SLE) nephritis presenting with both nephrotic syndrome (NS) and acute renal failure (ARF) demonstrated atypical fibrillary deposits in the glomerular mesangium and subendothelium. The size and morphology of fibrils resembled those of fibronectin (FN) glomerulopathy [1,2], as also confirmed by immunoperoxidase staining. As no familial history of FN disorders was noted, this case may represent the first report of a new kidney disease entity in the context of SLE.

Purpose Thyroid malignancies can be treated by surgery followed by ablation of the remnant tissue with 131I. As iodide removal from the body occurs by renal extraction, in patients suffering from end-stage renal disease it is necessary to properly evaluate both timing and method of the extracorporeal treatment. Methods We present two patients on regular hemodialysis, admitted in isolation to the Nuclear Medicine Department and treated with 131I for thyroid carcinoma diagnosed during the check-up for transplantation. Both patients underwent two hemodialysis sessions with a portable machine for CRRT (continuous renal replacement therapy), 24 and 48 hours after the administration of 50 mCi of 131I. The nursing staff were monitored with a dosimeter. Radioactivity of the patients, dialysate and urines were measured during hemodialysis. Results The greater reduction was obtained with the first dialysis, but in both patients a further, though shorter, hemodialysis at 48 hours was necessary for reaching a patient's radioactivity compatible with discharge. Radioactivity measured in the dialysate demonstrated the almost total removal of radioiodine by dialysis alone. In both patients, follow-up exams revealed a complete ablation of thyroid tissue, without signs of local recurrence. The dose of radioactivity of the dialysis staff was below allowable limits. Conclusions We conclude that a successful reduction of radioactivity, without dispersing its therapeutic efficacy, can be obtained with daily hemodialysis with a CRRT machine in patients in isolation treated with 131I. A therapeutic model is proposed.

Kidney involvement can be a serious complication of hematopoietic stem cell transplantation. In this Case Study, Fofi and colleagues describe a rare case of focal segmental glomerulosclerosis occurring as a complication of chronic graft-versus-host disease following peripheral blood stem cell transplantation. Background. A 54-year-old man with multiple myeloma underwent peripheral blood stem cell transplantation (PBSCT) with cells donated by his human leukocyte antigen (HLA)-identical sister. Eight months after PBSCT, the patient experienced chronic graft-versus-host disease with skin involvement (generalized erythema), mucosal ulceration, sicca syndrome, and elevated liver enzymes. Two years after PBSCT, the patient developed nephrotic syndrome with massive proteinuria, which required hospitalization. Investigations. Physical examination, blood and urine analyses, liver function tests, 24 h urinary albumin excretion and renal biopsy. Diagnosis. Focal segmental glomerulosclerosis as a complication of graft-versus-host disease. Management. Prednisone, ciclosporin and an angiotensin-converting-enzyme inhibitor.

The finding of increased levels of immunoglobulin A (IgA) against food antigens in patients with IgA nephropathy prompted the hypothesis of an association between IgA nephropathy and celiac disease (CD). Attention was initially directed to antigliadin antibodies, then to IgA antiendomysial antibodies (IgA-EMA). IgG1-EMA have been found in patients with CD with IgA-EMA-negative results. The presence of IgA- and IgG1-EMA was investigated in 36 patients with IgA nephropathy, 15 patients with other primary glomerulonephritis, and 15 patients with lupus nephritis. IgA-EMA and IgG1-EMA were detected by indirect immunofluorescence analysis. At the time of renal biopsy, the following factors were evaluated: history of macroscopic hematuria, serum creatinine level, urinalysis, 24-hour proteinuria, blood pressure, and histological classification of IgA nephropathy. Sixteen of 36 patients with IgA nephropathy (44.4%) showed EMA positivity. Among patients with positive EMA, 12 patients (75%) were IgG1-EMA positive, 2 patients (12.5%) were IgA-EMA positive, and 2 patients (12.5%) were positive for both isotypes. No significant differences were observed between the two groups (EMA positive versus EMA negative) concerning age, serum creatinine level, macroscopic hematuria, blood pressure, 24-hour proteinuria, or degree of renal histological involvement. IgA- and IgG1-EMA were not detected in patients with other primary nephropathies or lupus nephritis. These results, based on the finding of IgG1-EMA, suggest a common pathogenetic pathway for CD and IgA nephropathy. On this basis, the presence of IgG1-EMA and/or IgA-EMA should be investigated in patients with IgA nephropathy. Furthermore, the role of a gluten-free diet in the natural history of IgA nephropathy, at least in EMA-positive patients, needs to be ascertained.