Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus.

BACKGROUND: The hyperosmolar hyperglycemic state (HHS), an acute complication of diabetes mellitus with plasma hyperosmolarity, promotes the secretion of anti-diuretic hormone (ADH) and reduces the storage of ADH. Magnetic resonance T1-weighted imaging reflects ADH storage in the posterior pituitary lobe, which disappears when the storage is depleted. Whether the HHS induces ADH depletion leading to clinical manifestations has been unclear. CASE REPORT: A 55-year-old Japanese woman was admitted to our center because of mental disturbance and hypotension. She had received lithium carbonate for bipolar disorder and presented with polydipsia and polyuria from 15 years of age. On admission, she had mental disturbance (Glasgow Coma Scale, E4V1M1), hypotension (systolic blood pressure, 50 mmHg), and tachycardia (pulse rate, 123/min). Plasma glucose was 697 mg/dL osmolality was 476 mOsm/kg•H2O, and bicarbonate was 23.7 mmol/L. The diagnoses of HHS and hypovolemic shock were made. During treatment with fluid replacement and insulin therapy, the urine volume continued to be approximately 3 to 4 L/day, and an endocrine examination revealed ADH insufficiency and nephrogenic diabetes insipidus. Desmopressin 10 µg/day and trichlormethiazide 2 mg/day were necessary and administered, and the endogenous ADH secretion improved gradually. The signal intensity of the pituitary posterior lobe, initially decreased on magnetic resonance T1 images, was also improved. CONCLUSION: This patient had ADH insufficiency associated with ADH depletion due to hyperosmolarity and nephrogenic diabetes insipidus. Clinicians should be aware of the risk of the development of critical HHS and relative ADH insufficiency in patients being treated with lithium carbonate.

Extrapulmonary tuberculosis presented as fever of unknown origin in two patients with endstage kidney disease not on dialysis: usefulness of 18-FDG-PET/CT in the diagnostic localization of fever of unknown origin.

Tuberculosis is one of the common causes of fever of unknown origin in patients with chronic kidney disease (CKD). Extrapulmonary tuberculosis is more common in CKD patients, and is, unfortunately, often underdiagnosed despite extensive assessments. Recently, fluorine-18-deoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) has been available in the diagnosis of malignancy, inflammatory and infectious diseases, and has become a useful diagnostic tool. Here, we present two cases of endstage kidney disease who presented with fever of unknown origin at the time of dialysis initiation. In both cases, although interferon-gamma-releasing assay was positive, combined conventional diagnostic modalities such as computed tomography and gallium-citrate scintigraphy failed to detect the sites infected with tuberculosis. By contrast, extrapulmonary lesions were detected by FDG-PET/CT and successfully treated with combined anti-tuberculous drugs. Diagnosis of extrapulmonary tuberculosis was confirmed by biopsy of the affected lymph node and lumbar spine, followed by PCR of the biopsied specimen. These cases highlight the importance of considering tuberculosis as one of the differential diagnoses in pre-dialysis CKD patients with persistent fever, and the usefulness of FDG-PET/CT in the detection of infectious sites of extrapulmonary tuberculosis.

Osteomalacia secondary to renal tubular acidosis due to Sjögren's syndrome: a case report and review of the literature.

A 43-year-old woman was admitted to our hospital because of generalized bone pain. Arterial blood gas showed pH 7.266, HCO3- 13.5 mEq/l, and anion gap (AG) 12. Since her urine pH was 7.0 despite metabolic acidosis with normal AG, we diagnosed distal renal tubular acidosis (RTA). Serum phosphate was 2.5 mg/dl, the level of ß2 microglobulin was 41100 µg/l, and aminoaciduria was present. These results indicated proximal tubular dysfunction. The radiograph showed pseudofracture in the pubic bone, indicating osteomalacia. Bone scintigram showed abnormal accumulations of 99mTc-HMDP in multiple joints. Then, her generalized bone pain was considered to be a symptom of osteomalacia. Despite the absence of overt Sicca syndrome, the evaluation of Sjögren's syndrome (SjS) as a cause of distal RTA was performed. Antibodies to the SS-A level was 127U/ml. Tear break-up time was 3 s bilaterally and salivary gland scintigraphy showed low uptake of 99mTc in the submandibular glands and the parotids. Thus, we diagnosed SjS finally. Gallium scintigraphy showed mild abnormal uptake in bilateral kidneys, suggesting acute tubulointerstitial nephritis. After treatment with prednisolone, alfacalcidol, and sodium bicarbonate, bone pain was remarkably relieved. Additionally, aminoaciduria disappeared and the level of ß2 microglobulin decreased. We speculated that the coincidence of proximal tubular dysfunction and distal RTA cause a severe manifestation of osteomalacia.

LDL apheresis for cholesterol embolism following coronary artery bypass graft surgery--a case report.

A 76-year-old man without any prior history of abnormal urinalysis findings or renal insufficiency demonstrated mild renal dysfunction after coronary bypass graft surgery (CABG). Two months after CABG, pain and blueness in the toes (blue toe syndrome) appeared and, the serum creatinine level (S-Cr) increased from 1.2 to 2.0 mg/dL. On admission (3 months later), the urinary protein level was 0.5 g/day, white blood cell count 8,300/microL with eosinophils (Eo) 10.5%, S-Cr 2.1 mg/dL, and low-density lipoprotein (LDL) 106 mg/dL. Acute renal failure and blue toe syndrome due to a cholesterol embolism (CE) were diagnosed. Alprostadil 40 microg/day orally for 2 weeks and alprostadil 40 microg/day intravenously were used for 5 weeks, and Eo were 250/microL, S-Cr 2.5 mg/dL; however, blue toe syndrome gradually developed. At 8 weeks after admission, limaprost alfadex 30 microg/day orally was used for 3 weeks. However, the Eo gradually rose to 1,520/microL, S-Cr to 3.0 mg/dL, and LDL to 135 mg/dL, and LDL apheresis was therefore performed 20 times for CE. The data just after LDL apheresis was performed 10 times were as follows: Eo 1,120/microL, S-Cr 4.0 mg/dL, and LDL 89 mg/dL, and blue toe syndrome had disappeared. At 10 months after the first LDL apheresis, the Eo were 630/microL, S-Cr 2.9 mg/dL, and LDL 109 mg/dL. As a result, LDL apheresis was found to be beneficial for the treatment of CE with acute renal failure and blue toe syndrome after CABG.

Successful treatment of six patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure.

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure. We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration. The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 +/- 26 (mean +/- SD) mg/dL, serum creatinine 9.1 +/- 2.1 mg/dL, serum creatine phosphokinase 229,720 +/- 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 +/- 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration. As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.

Infusion of radiocontrast agents induces exaggerated release of urinary endothelin in patients with impaired renal function.

BACKGROUND: The aim of the study was to examine the role of endothelin in radiocontrast-induced nephropathy (RCN) in patients with chronic renal failure. METHODS: We measured plasma endothelin-1 (ET) and the urinary excretion of endothelin-like immunoreactivity before and after infusion of radio contrast medium (CM) in patients with normal renal function (group N; n = 6; mean serum creatinine concentration, 0.8 +/- 0.1 (SEM) mg/dl), and in another group, with renal dysfunction (group R; n = 6; 2.7 +/- 0.5 mg/dl). Half-normal saline (0.45% NaCl solution) was continuously infused in all patients for 25 h, at a rate of 100 ml/h; starting from 5 h before the infusion of CM. RESULTS: Plasma ET in group R (5.2 +/- 1.4 pg/ml) was significantly higher than in group N (0.9 +/- 0.3; P << 0.01). Urinary endothelin excretion corrected by creatinine concentration (uET/Cr) in group R (7.9 +/- 2.4 mg/g Cr) was significantly higher than in group N (1.5 +/- 0.4 mg/g Cr; P << 0.05). Urinary excretion levels of N-acetyl-Beta- d-glucosaminidase (NAG) and Beta2-microglobulin (Beta2M) were also significantly higher in group R (0.8 +/- 0.2 mU/g Cr and 670 +/- 400 mg/g Cr, respectively) than in group N (0.3 +/- 0.1 and 7.5 +/- 2.2, respectively). After CM infusion, uET/Cr in group R significantly increased, to 10.7 +/- 2.6 mg/g Cr on the next day and returned to baseline level on the third day. NAG and Beta2M showed a similar pattern, but a significant change in NAG was observed on the second day in group R. In group N, uET/Cr, NAG, and Beta2M did not change after CM infusion. Plasma ET remained unchanged throughout the observation period of 4 days in both groups. No patient developed pulmonary edema or a significant rise in serum creatinine (more than 0.5 mg/dl), caused by infusion of the amount of half-normal saline used. CONCLUSIONS: In the present study, uET/Cr increased after the administration of CM only in the patients with renal impairment. This difference in endothelin reaction may be a causal one, in that patients with renal insufficiency readily develop RCN. The infusion of half-normal saline starting before CM infusion causes no side effects and is safe for the prevention of CM-induced acute renal failure. The aim of the study was to examine the role of endothelin in radiocontrast-induced nephropathy (RCN) in patients with chronic renal failure.