Potassium metabolism in continuous ambulatory peritoneal dialysis patients

Background: Hypokalemia is common and may have contributed to the poor clinical outcome in peritoneal dialysis (PD) patients. In this study, we made a detailed investigation on the potassium metabolism in continuous ambulatory peritoneal dialysis (CAPD) patients and tried to find out the possible factors associated with the high prevalence of hypokalemia in PD patients. Methods: A cross-sectional survey in 243 clinically stable CAPD patients was made in our PD center in 2010. Patients were divided into four groups according to whether they were anuric or not and different dialysis regimens. Patients’ demographic data and data on potassium metabolism including dietary potassium intakes, residual renal potassium, and peritoneal dialysis potassium removal were collected. Results: The average potassium intake in our 243 PD patients was 32.1?±?11.1?mmol/day. The total potassium removal was significantly higher in non-anuric patients as compared to anuric patients (33.2?±?9.1 vs. 23.0?±?4.7?mmol/day for 3 exchanges per day and 35.2?±?8.9 vs. 28.6?±?6.3?mmol/day for 4 exchanges per day, respectively, p?p?p?p?R² linear?=?0.645, p?Conclusions: Our study suggested that if potassium intake was limited in PD patients, we should be aware of the risk of hypokalemia with high doses of PD when patients have good RRF. Our study also suggested that potassium removal in PD patients may not necessarily reflect potassium intake even if serum potassium is normal, the effect of ICW should be considered when evaluating potassium homeostasis.     

Acute renal failure due to uterine prolapse: a case report

Abstract

Herein, we present a successfully treated case with acute renal failure due to ureteral obstruction caused by total uterine prolapsed. A 55-year-old female patient presented to our hospital with the complaints of protrusion of the uterus for the last 3 months, pollakiuria, nocturia, decreased urine volume, and swelling of her body for the last week, and as well as impaired general status with shortness of breath for the last several days. Her physical examination revealed a blood pressure of 140/90?mmHg, pulse rate of 80 beats/min, body temperature of 37.8?°C, as well as uterine prolapse with infection and erosion on the surface of the uterus, crepitating rales in the basal segments of both lungs, and pretibial edema. Results of laboratory analyses were as follows: BUN?=?70?mg/dL, Cr?=?6.5?mg/dL, CRP?=?8.7?mg/dL, and leukocyte?=?12,000/mm³. Blood gas analysis revealed a pH of 7.35 and bicarbonate level of 14?mmol/L. Data obtained from ultrasonography, DTPA scintigraphy, and abdominal CT, which were performed assuming that the patient had post-renal renal failure due to the compression by uterus, supported this assumption. Bilateral nephrostomy catheters were inserted and appropriate fluid-electrolyte therapy for volume status and antibiotherapy were commenced. Renal functions returned to normal levels on the 4th day of therapy and her complaints disappeared. The patient underwent total abdominal hysterectomy and was monitored in terms of renal functions and diuresis. The present case was presented due to its importance for being a quite rare case who dramatically responded to accurate intervention performed in time.     

Transmission of LDLR Mutation From Donor Through Liver Transplantation Resulting in Hypercholesterolemia in the Recipient

Donor‐transmitted disease in organ transplantation is uncommon, but possible. The LDL receptor (LDLR), a key regulator of lipoprotein metabolism, is abundant in the liver. Mutations in the LDLR gene, leading to reduced LDLR activity, are the main cause for familial hypercholesterolemia (FH). The estimated prevalence of FH is 1/200–1/500 in the population indicating that there are 14–34 million individuals with FH worldwide. We describe a patient who developed severe hypercholesterolemia after liver transplantation (LT). The 42‐year‐old female, who was transplanted because of hepatic epithelioid hemangioendothelioma with normal liver function, exhibited an increase in plasma total cholesterol from 5.6 mmol/L (217 mg/dL) pretransplant to 11.7 mmol/L (452 mg/dL) at 6 months posttransplant. The respective increase in LDL cholesterol was from 3.30 (128 mg/dL) to 8.99 mmol/L (348 mg/dL). At 1 year, total and LDL cholesterol levels were 11.0 (425 mg/dL) and 7.81 (302 mg/dL), respectively. Sequencing of the coding region of LDLR from a liver graft biopsy revealed a splicing heterozygous mutation of LDLR, whereas no FH‐related mutation was found in DNA extracted from the patient's blood white cells. This confirmed the first reported case of a patient receiving a mutation in LDLR through LT. The case shows that a donor‐transmitted disorder should not be overlooked as a possible cause for severe hypercholesterolemia.     

Intensified treatment of hyperphosphatemia associated with reduction in parathyroid hormone in patients on maintenance hemodialysis

Background: This study investigated the therapeutic effect of intensive phosphorus-lowering therapy on intact-parathyroid hormone (iPTH) levels in hemodialysis patients.

Methods: Ninety-five hemodialysis patients with serum phosphorus ≥1.78?mmol/L and iPTH ≥300?pg/dL were apportioned to either the treatment or control group (n?=?43 and 52, respectively) based on patient commitment to treatment. The treatment group was given phosphorus-lowering therapies with phosphate binders (lanthanum, sevelamer or/and calcium reagent) combined with dietary phosphate restriction and intensified hemodialysis. The control individuals were given low doses of calcium agents, if serum calcium was <2.54?mmol/L. Percent changes in serum phosphorus and iPTH levels were compared between the two groups. In addition, based on the time required to achieve >20% decrease in serum phosphorus, the patients in the treatment group were further stratified as rapid responders (≤2?months; 27 patients) or slow responders (>2?months; 16 patients) and percent changes in iPTH were compared.

Results: Serum phosphorus and iPTH levels decreased from baseline in the treatment group (?24.08?±?1.93% and ?9.92?±?3.70%, respectively) but increased in the control group (22.00?±?3.63% and 104.21?±?23.89%; both p?p?Conclusions: For these patients on maintenance hemodialysis, intensive treatment of hyperphosphatemia was associated with a decrease in iPTH levels, especially for those who had achieved substantial reduction in serum phosphorus within 2?months.     

Second to fourth digit ratio, adult testosterone level and testosterone deficiency

Study Type – Diagnostic (exploratory cohort) Level of Evidence 2b What’s known on the subject? and What does the study add? 2D/4D digit ratio is inversely related to intrauterus exposure to androgens. Our experience suggests that 2D/4D digit ratio inversely predicts adult testosterone levels and is directly related to hypogonadism.

OBJECTIVES

? The ratio of the second and fourth finger lengths (2D/4D) is related to intrauterine exposure to testosterone. The relationship between 2D/4D and adult hormonal pattern is controversial. ? The aim of our study was to determine if there was a relationship between adult serum testosterone levels and the 2D/4D ratio.

PATIENTS AND METHODS

? We prospectively recruited 204 consecutive patients referred for transrectal prostate biopsy between January 2008 and June 2009. The same physician performed clinical examinations, 2D/4D measurements and the transrectal biopsy in all cases. ? Cut‐off points of 231 and 346 ng/dL testosterone (8 and 12 nmol/L) were used. 2D/4D determination was done with a vernier calliper on the left hand. ? The hormonal profile (testosterone and sexual hormone binding globulin) of the patients was determined between 7.00 am and 11.00 am. ? Age, weight, height, body mass index, toxic habits, digital rectal examination, prostate‐specific antigen and 2D and 4D measurements were recorded prospectively.

RESULTS

? The mean age was 67 ± 7 years and the mean testosterone level was 413 ± 18 ng/dL (14.33 ± 0.62 nmol/L). ? The percentages of patients with testosterone <231 ng/dL (8 nmol/L) and testosterone <346 ng/dL (12 nmol/L) were 6.1 and 30.6 respectively. ? Univariate analysis showed that low 2D/4D ratios were related to higher levels of testosterone (B=?741.98; β=?0.165, P= 0.045) and also with low prevalence of biochemical hypogonadism (testosterone <346 ng/dL). ? Mean 2D/4D ratio in patients with testosterone >346 ng/dL was lower than in patients with testosterone <346 ng/dL (2D/4D 0.97 ± 0.037 vs 0.99 ± 0.043 depending on their hormonal status, P= 0.05). High 2D/4D ratio was associated with low testosterone serum levels (P= 0.046).

CONCLUSIONS

? The 2D/4D ratio is related to adult testosterone levels and the presence of testosterone deficiency syndrome. ? Patients with high 2D/4D ratios have lower testosterone levels and higher risk of testosterone deficiency syndrome.     

The pre-transplant anemic condition is independent of long-term outcome in living-related kidney transplantation

The relationship between pre-transplant Hemoglobin (Hb) concentration and long-term outcome of living-related kidney transplantation is far from well addressed. A retrospective cohort study was conducted by reviewing the medical profile of the patients who received living-related kidney transplantations at our center from January 2006 to January 2013. Patients were divided into two groups: high Hb group (≥10?g/dL) and low Hb group (<10?g/dL). Cox regression model was utilized to analyze the effect of pre-transplant hemoglobin concentration on the patient and graft survival. About 422 patients were of Hb level <10?g/dL (78.30?±?14.18?g/dL), 280 were >10?g/dL (116.2?±?14.43?g/dL) (p?p?=?0.096; and 4.04% vs. 2.14%, p?=?0.165, respectively). Cox regression model revealed that pre-transplant Hb level <10?g/dL was independent of increased overall mortality (HR?=?3.379; 95% CI: 0.706–17.172) and increased death censored allograft failure risk (HR?=?1.556; 95% CI: 0.595–4.069). Pre-transplant Hb concentration <10?g/dL is independent of poor long-term outcome of living-related kidney transplantation.     

Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women

The dietary acid load created by the typical Western diet may adversely impact the skeleton by disrupting calcium metabolism. Whether neutralizing dietary acid with alkaline potassium salts results in sustained improvements in calcium balance remains controversial. In this randomized, double‐blind, placebo‐controlled study, 52 men and women (mean age 65.2 ± 6.2 years) were randomly assigned to potassium citrate 60 mmol/d, 90 mmol/d, or placebo daily with measurements of bone turnover markers, net acid excretion, and calcium metabolism, including intestinal fractional calcium absorption and calcium balance, obtained at baseline and at 6 months. At 6 months, net acid excretion was significantly lower in both treatment groups compared to placebo and it was negative, meaning subjects' dietary acid was completely neutralized (?11.3 mmol/d on 60 mmol/d; ?29.5 mmol/d on 90 mmol/d, p < 0.001 compared to placebo). At 6 months, 24‐hour urine calcium was significantly reduced in persons taking potassium citrate 60 mmol/d (?46 ± 15.9 mg/d) and 90 mmol/d (?59 ± 31.6 mg/d) compared with placebo (p < 0.01). Fractional calcium absorption was not changed by potassium citrate supplementation. Net calcium balance was significantly improved in participants taking potassium citrate 90 mmol/d compared to placebo (142 ± 80 mg/d on 90 mmol/d versus ?80 ± 54 mg/d on placebo; p = 0.02). Calcium balance was also improved on potassium citrate 60 mmol/d, but this did not reach statistical significance (p = 0.18). Serum C‐telopeptide decreased significantly in both potassium citrate groups compared to placebo (?34.6 ± 39.1 ng/L on 90 mmol/d, p = 0.05; ?71.6 ± 40.7 ng/L on 60 mmol/d, p = 0.02) whereas bone‐specific alkaline phosphatase did not change. Intact parathyroid hormone was significantly decreased in the 90 mmol/d group (p = 0.01). Readily available, safe, and easily administered in an oral form, potassium citrate has the potential to improve skeletal health. Longer‐term trials with definitive outcomes such as bone density and fracture are needed. © 2013 American Society for Bone and Mineral Research.     

Severe hyperkalemic type 4 renal tubular acidosis after kidney transplantation: a case report

BACKGROUND: Hyperkalemia after transplantation is a common event, occurring in up to 70% of patients. It is usually asymptomatic but sometimes manifests as muscle weakness or cardiac arrhythmias. METHODS: Case report. RESULTS: At 102 days after a second cadaveric kidney transplantation, a 15-year-old boy, was admitted to the emergency room with severe muscle weakness. His examinations showed a serum potassium of 9.8 mEq/L; blood pH 7.1; serum bicarbonate 7.6 mmol/L; and creatinine 2.5 mg/dL. He was initially treated with sodium bicarbonate, calcium gluconate, and furosemide. Subsequent investigation showed hyperchloremic metabolic acidosis, urinary pH <5.5, positive urinary anion gap, reduced transtubular potassium gradient (TTKG, 1.5) and low levels of aldosterone (0.7 ng/mL), suggesting the presence of type 4 renal tubular acidosis (RTA). Other causes of hyperkalemia were excluded in the present case. Serum levels of potassium returned to normal when fludrocortisone was added to the bicarbonate supplementation. This case of severe hyperkalemic secondary to type 4 RTA after kidney transplantation only responded to the combination of alkali and mineralocorticoid therapies.     

Hypothesis: a simple algorithm to distinguish between hypoaldosteronism and renal aldosterone resistance in patients with persistent hyperkalemia

Aim: Many patients with hyperkalemia have a readily identifiable cause, which leads to appropriate management. In others, particularly those with a reduced glomerular filtration rate, differentiating between (relative) hypoaldosteronism (HA) and renal aldosterone resistance (RAR) can be problematic. The aim of this study was to see if a plasma aldosterone to potassium algorithm could be defined which would help identify patients with hyperkalemia owing to suboptimal levels of aldosterone, thereby validating treatment with 9-alpha-fluhydrocortisone, instead of cation exchange resins, if more conservative treatment fails. Methods: A literature search for, and analysis of, studies providing details of plasma aldosterone and plasma potassium in normals (made hyperkalemic)and patients with a plasma potassium >5.3 mmol/L, and a contemporaneous plasma aldosterone. Results: One study was found in which normals were made significantly hyperkalemic (to 6.3 mmol/L). These subjects, while on a high sodium, low potassium (western) diet (n = 5), provided an arbitrary definition of a simple aldosterone to potassium algorithm for diagnosis (factored aldosterone (FAldo) = plasma aldosterone/(plasma K – 4.2)). The limit for FAldo is set at 280(pmol/L) or 10(ng/dL): results below the limit suggest HA; above the limit, RAR. This algorithm was then tested against, and, when plasma potassium was greater than 5.3, found to be consistent with, reported patients with confirmed HA (n = 33) and pseudohypoaldosteronism (n = 23). The ratios in reported patients with renal failure (n = 43) were consistent with either HA (n = 30) or RAR(n = 13). Hypothesis: In hyperkalemic patients a plasma aldosterone to potassium algorithm may help distinguish HA from RAR, thereby guiding therapy.     

Outcome of renal transplantation from older living donors compared to younger living donor in developing country

Objectives: To evaluate whether the outcomes of renal grafts from living related donors older than 60 years are acceptable, in terms of renal function and patient/graft survival. Material and methods: One hundred and forty-seven patients who received kidneys from donor age ≥60 years constituted the study group (group 1). The control group (group 2) consisted of 1310 patients who received renal transplants from donor age <60 years. Outcome measures included graft, patient survival, acute rejection rate and serum creatinine (SCr) in patients/donors. Graft and patient survivals were compared using the Kaplan–Meier method. Results: The mean age of donors was 62.7?±?3.39 years in group 1 and 43.45?±?9.65 years in group 2. Patient survival at 1, 3 and 5 years was 95.7%, 89.4% and 82.6% in group 1 and 93.8%, 89.1% and 83.1% in group 2 (p?=?0.785), respectively. Death-censored graft survival at 1, 3 and 5 years was 98.5%, 94.8% and 94.8% in group 1 and 96.1%, 92.9% and 89% in group 2 (p?=?0.166), respectively. Biopsy-proven acute rejections were 21% and 16.8% (p?=?0.206) and chronic rejections 5% and 3.4% in group 1 and 2, respectively (p?=?0.542). Recipient SCr (mg/dL) was 1.8?±?0.31 in group 1 and 1.58?±?0.37 in group 2. The donor SCr levels at the last follow-up were 1?mg/dL and 0.9?mg/dL in group 1 and 2, respectively. Conclusions: Donor age did not affect patient and graft survival in the 5-year follow-up in our study. Age alone seems not to be an exclusion criterion to living kidney donation.     

Hyperuricemia predicts adverse clinical outcomes after cardiac resynchronization therapy

Abstract

Objectives: Changes in the levels of serum creatinine and N-terminal of prohormone brain natriuretic peptide (NT-proBNP) are useful risk markers after cardiac resynchronization therapy (CRT). The diagnostic value of changes in serum uric acid levels has been established in chronic heart failure, but no data are available on the prognostic value of hyperuricemia in a CRT population. Design: We measured markers of renal function [creatinine, blood urea nitrogen (BUN) and uric acid] and NT-proBNP levels of 129 heart failure patients undergoing CRT in a prospective, observational study. The 5-year all-cause mortality and the 6-month clinical response (≥ 15% increase in the left ventricular ejection fraction) were considered as study end points. Results: In multivariable analyses, the uric acid was found to be a statistically significant predictor of the outcome. Uric acid levels exceeding 386?mmol/L before CRT increased the chances of mortality [n?=?55, hazard ratio?=?2.39 (1.30-4.39), p?<?0.01] and poor clinical response [n?=?37, odds ratio?=?2.89 (1.22-6.87), p?=?0.01] independently of serum NT-proBNP and other factors. Conclusions: Elevated uric acid concentrations in patients with CRT are associated with an increased risk of mortality and poor clinical response independently of the NT-proBNP levels and other relevant clinical factors.     

Meta-analysis of statin therapy in maintenance dialysis patients

Abstract

The effects of statin therapy in patients on maintenance dialysis remained uncertain. We conducted a meta-analysis to investigate the effects of statin on major clinical outcomes. We systematically searched Pubmed, Web of Science, Cochrane Library, Chinese National Knowledge Infrastructure, Wanfang and Chinese Technological Journal of Database for randomized controlled trials (RCTs). Criteria for inclusion were RCTs on statins therapy versus placebo, >3 months of follow-up. The outcomes were serum level of low density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), triglyceride (TG), high-sensitivity C-reactive protein (hs-CRP) and albumin (ALB), all cardiac events, cardiovascular deaths and all-cause mortality. Twenty-one trials were identified, providing data for 8186 patients on maintenance dialysis. Statin therapy reduced LDL-C (weighted mean difference [WMD]?=??0.74?mmol/L; 95%CI [?0.96,??0.52], p?<?0.00001), TG (WMD?=??0.36?mmol/L; 95%CI [?0.57,??0.14], p?=?0.001), and hs-CRP (WMD?=??3.98?mg/L; 95%CI [?5.24,??2.72], p?<?0.00001), elevated HDL-C (WMD?=?0.25?mmol/L; 95%CI [0.10,?0.39], p?=?0.0007) and ALB (WMD?=?1.70?g/L; 95%CI [0.19,?3.21], p?=?0.03) significantly comparing with placebo. Statin therapy also had benefit in reducing all cardiac events (relative risk [RR]?=?0.90; 95%CI [0.83,?0.97], p?=?0.006), but had no effect on cardiovascular deaths (RR?=?0.97; 95%CI [0.88,?1.07], p?=?0.54) or all-cause mortality (RR?=?0.98; 95%CI [0.93,?1.04], p?=?0.49). In conclusion, statins had no impact on all-cause or cardiovascular mortality, while there was an overall significant improvement for dyslipidemia, hs-CRP, hypoalbuminemia and cardiovascular events in dialysis patients.     

Do We Overtreat Post-Thyroidectomy Hypocalcemia?

Background

Calcium and calcitriol supplements are standard for patients with post-thyroidectomy serum calcium <2.0?mmol/L; however, we wondered whether we overtreat post-thyroidectomy hypocalcemia with intraoperative parathyroid hormone (PTH). We examined quick-intraoperative intact PTH (QiPTH) assay results to find a suitable treatment for post-thyroidectomy hypocalcemia.

Methods

We studied 197 bilateral thyroidectomy patients. Post-thyroidectomy hypocalcemia was defined as serum calcium <2.0?mmol/L. A QiPTH assay was done 15?min after the thyroidectomy (QiPTH₁₅), and hypoparathyroidism was defined as PTH <15?ng/L. The QiPTH₁₅ assay was used to determine the effects of the thyroidectomy on postoperative PTH levels and serum calcium levels. The natural course and medical response of hypocalcemia was observed in patients with a QiPTH₁₅ ≥15?ng/L.

Results

None of the 187 patients with a QiPTH₁₅ ≥15?ng/L developed postoperative hypoparathyroidism. However, 79 patients developed transient hypocalcemia, and those with Graves’ disease (47/94) had significantly (p?Conclusions When post-thyroidectomy QiPTH₁₅ was ≥15?ng/L, postoperative hypoparathyroidism was excluded, but more than one-third of the patients developed post-thyroidectomy hypocalcemia. However, most of them recovered without treatment, and a few recovered after taking only a calcium supplement. We believe that using QiPTH₁₅ results as a guide will prevent overtreatment of post-thyroidectomy hypocalcemia.     

Effect of ionized serum calcium on outcomes in acute kidney injury needing renal replacement therapy: secondary analysis of the acute renal failure trial network study

Abstract

Background: Hypocalcemia is very common in critically ill patients. While the effect of ionized calcium (iCa) on outcome is not well understood, manipulation of iCa in critically ill patients is a common practice. We analyzed all-cause mortality and several secondary outcomes in patients with acute kidney injury (AKI) by categories of serum iCa among participants in the Acute Renal Failure Trial Network (ATN) Study. Methods: This is a post hoc secondary analysis of the ATN Study which was not preplanned in the original trial. Risk of mortality and renal recovery by categories of iCa were compared using multiple fixed and adjusted time-varying Cox regression models. Multiple linear regression models were used to explore the impact of baseline iCa on days free from ICU and hospital. Results: A total of 685 patients were included in the analysis. Mean age was 60 (SD?=?15) years. There were 502 male patients (73.3%). Sixty-day all-cause mortality was 57.0%, 54.8%, and 54.4%, in patients with an iCa <1, 1–1.14, and ≥1.15?mmol/L, respectively (p?=?0.87). Mean of days free from ICU or hospital in all patients and the 28-day renal recovery in survivors to Day 28 were not significantly different by categories of iCa. The hazard for death in a fully adjusted time-varying Cox regression survival model was 1.7 (95% CI: 1.3–2.4) comparing iCa <1 to iCa?≥?1.15?mmol/L. No outcome was different for levels of iCa?>?1?mmol/L. Conclusion: Severe hypocalcemia with iCa?<?1?mmol/L independently predicted mortality in patients with AKI needing renal replacement therapy.     

Contralateral suppression of aldosterone at adrenal venous sampling predicts hyperkalemia following adrenalectomy for primary aldosteronism

Background

We aimed to determine whether a greater degree of contralateral suppression of aldosterone secretion at adrenal venous sampling predicted the development of postoperative hyperkalemia after unilateral adrenalectomy for primary aldosteronism.

Altered hormonal activity in severely ill patients after injury or sepsis

We studied the hormonal millieu and possibility of altered thyroid function in 25 patients in a surgical intensive care unit (ICU) who had severe life-threatening illnesses. Sixteen patients had septic complications and nine patients had multiple-system injuries. On admission to the ICU, serial measurements were begun of thyroxine (T4), triiodothyronine (T3), T4-binding globulin, thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), cortisol, prolactin, human growth hormone, catecholamine, insulin and glucose, lactate, retinol-binding protein, prealbumin, and transferrin levels. All patients initially had low normal levels of T4 (4.5 +/- 2 micrograms/dL) and T3 (55 +/- 26 ng/dL), with normal TSH levels (2.3 +/- 2.3 microU/mL) (the "low T3 syndrome"). The 11 surviving patients had their levels increase to normal before leaving the ICU (T4, 7.0 +/- 2.1 micrograms/dL; T3, 110 +/- 48 ng/dL; and TSH, no change). The 14 patients who died showed further decreases before death (T4, 2.6 +/- 2.1 micrograms/dL; T3, 30.6 +/- 23.5 ng/dL; and TSH, 0.9 +/- 0.7 microU/mL). The corticotropin, cortisol, prolactin, and growth hormone levels were normal throughout the study. Catecholamine levels were high initially and decreased in surviving patients. Epinephrine levels increased greatly in nonsurvivors before death, and the norepinephrine-epinephrine ratio decreased from 5.7:1 to 2:1. After protirelin (thyroid-releasing hormone [TRH]) stimulation, the TSH level increased either minimally or not at all in six patients who eventually died. This indicates hypothalamic-pituitary dysregulation or suppression, and altered release and/or peripheral metabolism of T4. Whether this represents a deficiency of thyroid hormone for cell and organ function remains to be established.     

Low testosterone bioavailability is related to prostate cancer diagnose in patients submitted to prostate biopsy

Introduction

Relationship between prostate cancer (PCa) and testosterone (T) is controversial. Conflicting evidence has been published about T levels and development of PCa.

Aim

(1) To determine the relationship between hormone levels and the diagnosis of PCa. (2) To specifically focus on the relationship between PCa and T in men classified as biochemically hypogonadal.

Materials and methods

Prospective analysis of 1,000 transrectal ultrasound guided prostate biopsies (5?+?5 cores biopsies) between September 2007 and January 2010 in one center. Indication for prostate biopsy was suspicion of PCa on the basis of elevated prostate-specific antigen (PSA) and/or digital rectal examination (DRE). Serum testosterone and sex hormones binding globulin (SHBG) were determined in these patients. Of 557 men, the data were sufficient for further analysis. Age, body mass index (BMI), smoking/drinking habits, PSA, free PSA, PSA density, prostate volume, number of previous biopsies, DRE, and hormone levels were prospectively recorded.

Results

No relationship was found between T and PCa (449?±?167?ng/dL in PCa versus 437?±?169?ng/dL in non-PCa). SHBG was significantly higher in patients with PCa (51?±?27?ng/dL in PCa vs. 44?±?18?ng/dL in non-PCa). In hypogonadal men, T levels correlated with the PCa (235?±?95?ng/dL in men with PCa versus 270?±?58?ng/dL in men without PCa, P?=?0.004).

Conclusions

T levels were comparable in men with and without PCa, but SHBG levels were significantly higher in men with PCa. In men with low T, the men with PCa had a lower serum T levels and a lower prostate volume than the men without PCa.     

Rare cause of weight loss in a kidney transplant recipient: iron overload

Various reasons such as malignancies and chronic infections may cause weight loss in kidney transplant patients. In this report, iron overload as a rare cause of weight loss in a kidney transplant patient is presented. Forty-seven-year-old male patient who transplanted from a deceased donor 5 years ago was hospitalized because of 20?kg of weight loss. In medical history, he had history of hemodialysis for 89 months and received 100–300?mg of intravenous iron therapy per week before transplantation and transfused eight units of blood. In physical examination, weight and height were 45?kg and 185?cm, respectively. Respiratory and cardiac auscultation was normal. Laboratory results revealed as follow: glucose 76?mg/dL, urea 60?mg/dL, creatinine 1.35?mg/dL, aspartate aminotransferase 74?U/L, alanine aminotransferase 77?U/L, C-reactive protein 2.59?mg/dL, albumin 3.3?g/dL, globulin 3.4?g/dL, white blood cells 3200/mm³, hemoglobin 13.1?g/dL and platelets 190,000/mm³. Chest and abdominal tomography didn’t reveal any pathology. Portal Doppler ultrasound showed signs of early cirrhosis. Viral and autoimmune hepatitis markers were negative. Ferritin was 5300?ng/mL and transferrin saturation was 82%. In liver biopsy, hemosiderosis was diagnosed and heterozygous H63D gene mutation was detected. Totally, 19 units of phlebotomy were performed. Liver function tests and serum ferritin decreased gradually. At outpatient follow-up in 6 months, he returned to former weight. In conclusion, there can be several causes of weight loss in kidney transplant patients. Iron overload can come across as a rare cause of weight loss. In these patients, ferritin levels should be checked and diagnosis should be clarified by liver biopsy and gene mutation analysis.     

Tubulointerstitial nephritis and uveitis syndrome with transient hyperthyroidism in an elderly patient

A 69-year-old Japanese woman without any specific medical or family history was admitted to our hospital for renal insufficiency with proteinuria. On laboratory examinations, deteriorated renal function (blood urea nitrogen level was 34.9 mg/dL and creatinine level was 1.78 mg/dL) and elevated urinary levels of N-acetyl-β-d-glucosaminidase (23.4 U/L) and β2-microgloblin (20200 μg/L) were observed. We performed a renal biopsy. The biopsied specimen showed severe diffuse infiltration of mononuclear cells into the interstitium, with normal glomeruli, and these findings were compatible with acute tubulointerstitial nephritis (ATIN). At that time, ATIN seemed to be idiopathic. We performed gallium scintigraphy, and the results revealed uptake by the bilateral kidneys, thyroid gland, and right parotid gland. Serum thyroid stimulating hormone (TSH) was undetectable, free triiodothyronine was normal (3.11 pg/mL), and free thyroxine was elevated to 2.4 ng/dL. The titers of antithyroglobulin and antithyroid microsomal and TSH-receptor antibodies were not elevated. Two months later, burning pain and conjunctival congestion developed in both eyes. She had uveitis, as diagnosed by slit-lamp examination. Topical corticosteroid was used for the uveitis with success. We could not detect any cause of the uveitis, so a diagnosis of tubulointerstitial nephritis and uveitis syndrome (TINU syndrome) with associated hyperthyroidism was made. Treatment was started with 15 mg/day of prednisolone. Now her renal function is slowly recovering. There are few reports of TINU syndrome with transient hyperthyroidism. This case suggests the possibility of thyroid dysfunction in patients with TINU syndrome. A laboratory evaluation of thyroid function should be considered in the diagnostic evaluation of TINU syndrome.     

Clomiphene citrate is safe and effective for long‐term management of hypogonadism

Study Type – Therapy (population cohort) Level of Evidence 2a What's known on the subject? and What does the study add? Clomiphene citrate (CC) has previously been documented to be efficacious in the treatment of hypogonadism. However little is known about the long term efficacy and safety of CC. Our study demonstrates that CC is efficacious after 3 years of therapy. Testosterone levels and bone mineral density measurement improved significantly and were sustained over this prolonged period. Subjective improvements were also demonstrated. No adverse events were reported.

OBJECTIVE

• ? To assess the efficacy and safety of long‐term clomiphene citrate (CC) therapy in symptomatic patients with hypogonadism (HG).

PATIENTS AND METHODS

• ? Serum T, oestradiol and luteinizing hormone (LH) were measured in patients who were treated with CC for over 12 months.
• ? Additionally, bone densitometry (BD) results were collected for all patients. Demographic, comorbidity, treatment and Androgen Deficiency in Aging Men (ADAM) score data were also recorded.
• ? Comparison was made between baseline and post‐treatment variables, and multivariable analysis was conducted to define predictors of successful response to CC.
• ? The main outcome measures were predictors of response and long‐term results with long‐term CC therapy in hypogonadal patients.

RESULTS

• ? The 46 patients (mean age 44 years) had baseline serum testosterone (T) levels of 228 ng/dL.
• ? Follow‐up T levels were 612 ng/dL at 1 year, 562 ng/dL at 2 years, and 582 ng/dL at 3 years (P < 0.001).
• ? Mean femoral neck and lumbar spine BD scores improved significantly.
• ? ADAM scores (and responses) fell from a baseline of 7 to a nadir of 3 after 1 year.
• ? No adverse events were reported by any patients.

CONCLUSIONS

• ? Clomiphene citrate is an effective long‐term therapy for HG in appropriate patients.
• ? The drug raises T levels substantially in addition to improving other manifestations of HG such as osteopenia/osteoporosis and ADAM symptoms.