Page kidney following spontaneous subcapsular hematoma immediately after kidney transplantation: a case report.

BACKGROUND: Page kidney (PK) is the occurrence of kidney hypoperfusion and ischemia due to pressure on the kidney by a subcapsular hematoma (SH), a mass, or fluid collection. SH after renal transplantation may result in kidney ischemia and graft loss. CASE PRESENTATION: We present a rare case of early spontaneous SH in an allograft kidney that led to a decrease in renal function. A 56-year-old male patient underwent deceased donor kidney transplantation. After declamping, appropriate renal perfusion and immediate diuresis were observed, with no evidence of SH. However, his urinary output abruptly decreased 6 h postoperatively. Abdominal ultrasonography showed 28 mm deep SH on transplant and the resistive index (RI) increased to 0.98-1 and diastolic flow reversal was observed. Surgical interventions were performed 2 days after transplantation, following a further decrease in urinary output. Serum creatinine decreased to 2.2 mg/dL, urinary output increased to an average of 200 cc per hour and the RI value was decreased to 0.7 on POD 7. CONCLUSION: In patients with abrupt decreased renal function after transplantation, SH should be suspected and the presence of PK should be determined using Doppler USG. In these cases, surgical intervention may avoid allograft dysfunction.

The neutrophil-to-lymphocyte ratio may indicate when to start hemodialysis.

We evaluated whether the neutrophil-to-lymphocyte ratio (NLR) could aid dialysis decision-making in combination with the clinical presentation and biochemical findings. We retrospectively evaluated the medical records of 279 patients who commenced chronic maintenance hemodialysis. We compared the laboratory findings at 6 months before dialysis to those at dialysis initiation. NLR cutoffs and risk factors for each of six uremic symptoms were determined. Mean age was 60.7 years and mean estimated glomerular filtration rate (eGFR) was 5.7 ± 2.5 mL/min/1.73 m2 at the time of hemodialysis and 7.7 ± 3.8 mL/min/1.73 m2 6 months earlier (p < 0.001). The mean NLR increased significantly from 2.5 ± 1.0 to 4.9 ± 2.8 (p < 0.001). The NLR was positively correlated with the C-reactive protein level (r = 0.202, p = 0.009) and negatively correlated with those of albumin (r = -0.192, p = 0.001) and total CO2 (r = -0.134, p = 0.023). The NLR cutoffs for neurological and gastrointestinal symptoms as determined using receiver operator curve analysis were 2.4 (area under the curve [AUC] 0.976; 95% confidence interval [CI] 0.960-0.993; sensitivity 92.2%; specificity 94.7%) and 3.6 (AUC 0.671; 95% CI 0.588-0.755; sensitivity 68.1%; specificity 63.5%), respectively. On multiple linear regression analysis of neurological symptoms, the NLR was a significant predictor (ß = -0.218, p = 0.017), as was age (ß = 0.314, p = 0.037). In conclusion, the NLR may serve as a supplementary marker predicting uremic symptoms and a need for hemodialysis in stage 5 CKD patients.

Human Endothelial Progenitor Cells Protect the Kidney against Ischemia-Reperfusion Injury via the NLRP3 Inflammasome in Mice.

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and progression to chronic kidney disease (CKD). However, no effective therapeutic intervention has been established for ischemic AKI. Endothelial progenitor cells (EPCs) have major roles in the maintenance of vascular integrity and the repair of endothelial damage; they also serve as therapeutic agents in various kidney diseases. Thus, we examined whether EPCs have a renoprotective effect in an IRI mouse model. Mice were assigned to sham, EPC, IRI-only, and EPC-treated IRI groups. EPCs originating from human peripheral blood were cultured. The EPCs were administered 5 min before reperfusion, and all mice were killed 72 h after IRI. Blood urea nitrogen, serum creatinine, and tissue injury were significantly increased in IRI mice; EPCs significantly improved the manifestations of IRI. Apoptotic cell death and oxidative stress were significantly reduced in EPC-treated IRI mice. Administration of EPCs decreased the expression levels of NLRP3, cleaved caspase-1, p-NF-κB, and p-p38. Furthermore, the expression levels of F4/80, ICAM-1, RORγt, and IL-17RA were significantly reduced in EPC-treated IRI mice. Finally, the levels of EMT-associated factors (TGF-ß, α-SMA, Snail, and Twist) were significantly reduced in EPC-treated IRI mice. This study shows that inflammasome-mediated inflammation accompanied by immune modulation and fibrosis is a potential target of EPCs as a treatment for IRI-induced AKI and the prevention of progression to CKD.

Acute interstitial nephritis associated with ingestion of Achyranthes japonica extract: a case report.

BACKGROUND: The Japanese chaff flower, Achyranthes japonica, is used as complementary medicine to control degenerative arthritis. Although commonly used in South Korea, there has been no report of side effects. We report the first case of acute interstitial nephritis (AIN) that occurred in a woman who ingested A. japonica extract for 4 months. CASE PRESENTATION: A 56-year-old Korean woman was admitted for deterioration of renal function. She had general weakness and nausea for 1 month. Her initial blood urea nitrogen and serum creatinine levels were 26.3 mg/dL and 3.2 mg/dL, respectively. She acknowledged ingesting A. japonica extract for the past 4 months. Renal histology demonstrated AIN represented by immune cell infiltration into the interstitium, tubulitis, and tubular atrophy, but the glomeruli were intact. A. japonica was discontinued immediately and conservative management was started. Renal function was nearly restored to the baseline level without medication after 13 months. CONCLUSION: This is a rare case report of AIN associated with a pure A. japonica extract. In the case of unknown etiology of AIN, physicians should ask about the use of herbal medicines, nutraceuticals, and traditional folk medicines including A. japonica.

Lower serum sodium levels predict poor clinical outcomes in patients with insomnia.

BACKGROUND: The association between lower serum sodium levels and the clinical outcomes of insomnia patients remains unclear. We explored whether lower serum sodium is associated with poor clinical outcomes in patients with insomnia. METHODS: We retrospectively enrolled patients with a diagnosis of insomnia from January 2011 to December 2012. We divided participants into three groups according to initial serum sodium level: tertile 1 (< 138 mmol/L), tertile 2 (138.0-140.9 mmol/L), and tertile 3 (≥ 141.0 mmol/L). To calculate the relative risk of death, hazard ratios (HRs) and 95% confidence intervals (CIs) were obtained using Cox proportional hazard models. RESULTS: A total of 412 patients with insomnia were included, of whom 13.6% (n = 56) had hyponatremia. Patients with lower serum sodium concentrations were older and had lower hemoglobin, calcium, phosphorus, and albumin levels. At the median follow-up of 49.4 months, 44 patients had died and 62 experienced acute kidney injury (AKI). Kaplan-Meier analysis showed significantly higher mortality in patients in the lowest tertile for serum sodium. The lowest tertile of the serum sodium level and the AKI were associated with all-cause mortality. However, the lowest tertile of the serum sodium level was not significantly associated with AKI. CONCLUSIONS: The lowest tertile of the serum sodium level was associated with a higher mortality rate in insomnia patients. Our results suggest that the serum sodium level could serve as a prognostic factor in insomniacs; patients with lower sodium levels require particular care.

Erythropoietin Ameliorates Ischemia/Reperfusion-Induced Acute Kidney Injury via Inflammasome Suppression in Mice.

Acute kidney injury (AKI) is the most common condition in hospitalized patients. As ischemia/reperfusion-induced AKI (IR-AKI) is as a major contributor to end-stage disease, an effective therapeutic intervention for IR-AKI is imperative. Erythropoietin (EPO) is a potent stimulator of erythroid progenitor cells and is significantly upregulated during hypoxia. Here, we investigated the renoprotective effects of EPO in an IR-AKI mouse model. Mice were assigned to sham, EPO only, and IR only groups, and the IR group was treated with EPO prior to injury. EPO was administered twice at 30 min prior to bilateral renal artery occlusion, and 5 min before reperfusion, with all mice sacrificed 24 h after IR-AKI. The serum was harvested for renal functional measurements. The kidneys were subjected to histological evaluation, and the biochemical changes associated with renal injury were assessed. EPO significantly attenuated the renal dysfunction associated with IR-AKI, as well as tissue injury. Apoptotic cell death and oxidative stress were significantly reduced in EPO-treated mice. Macrophage infiltration and expression of ICAM-1 and MCP-1 were also significantly reduced in EPO-treated mice. Furthermore, the expression of inflammasome-related factors (NLRP1, NLRP3, and caspase-1 cleavage), via the activation of the COX-2 and NF-B signaling pathways were significantly reduced following EPO treatment. To our knowledge, this is the first study to demonstrate that inflammasome-mediated inflammation might be a potential target of EPO as a treatment for ischemic AKI.

A case report of successfully treated nephrotic syndrome after renal angioplasty.

BACKGROUND: The standard treatment of renovascular hypertension accompanying renal artery stenosis (RAS) consists of angioplasty and administration of antihypertensive medication. Although nephrotic syndrome (NS) has been reported to be associated with RAS, the development of NS after revascularization of RAS is extremely rare. CASE PRESENTATION: A 48-year-old man presented with uncontrolled hypertension and azotemia. The right kidney was atrophic, and RAS of the left kidney was suspected based on a post-captopril DTPA scan. His blood pressure stabilized after renal angioplasty; however, he complained of edema after 1 week. NS developed and was diagnosed as focal segmental glomerulosclerosis (FSGS) based on renal biopsy. He received an angiotensin receptor blocker. Proteinuria resolved after 1 year. CONCLUSIONS: FSGS rarely develops after angioplasty of renal artery stenosis. This is the first report of successful treatment of this condition using an angiotensin receptor blocker during 1-year follow-up.

Incidence, risk factors, and clinical outcomes of acute kidney injury associated with acute pyelonephritis in patients attending a tertiary care referral center.

Acute kidney injury (AKI) associated with acute pyelonephritis (APN) rarely has been reported. The aim of this study was to evaluate the incidence and risk factors of AKI associated with APN. We retrospectively reviewed the medical records of 403 patients over 18-year old age hospitalized for APN management from October 2009 to September 2014 in tertiary care referral center. Demographic data, clinical symptoms and signs, and laboratory findings were gathered from the medical records and analyzed. The mean age of patients was 57 years and APN commonly occurred in female (87.6%). AKI occurred in 253 patients (62.8%). As per the RIFLE classification, renal injury was graded as 'Risk' (62.1%), 'Injury' (26.5%), and 'Failure' (11.4%). AKI patients were more likely a male gender and had complicated APN. The AKI group had a significantly higher tendency to present with shock. The prevalence of underlying chronic kidney disease (CKD) was significantly higher in the AKI group. There was no difference in mortality between the AKI and non-AKI groups. Multivariate analysis revealed that age over 65 (OR 1.93, 95% CI 1.18-3.13, p= .008), complicated (OR 2.13, 95% CI 1.35-3.34, p= .001) and bilateral APN (OR 1.71, 95% CI 1.01-2.88, p= .045), and initial shock (OR 2.44, 95% CI 1.05-5.71, p= .039) were independent risk factors for the occurrence of AKI in patients with APN. Physicians should attempt to prevent, detect, and manage AKI associated with APN in patients with above conditions.

The aqueous extract of aged black garlic ameliorates colistin-induced acute kidney injury in rats.

The use of colistin in the treatment of multidrug-resistant Gram-negative bacterial infections is restricted due to nephrotoxicity. We investigated the effects of aged black garlic extract (ABGE) on colistin-induced kidney injury in rats. Rats were assigned to four groups. Normal saline was intraperitoneally and intragastrically injected for control group. ABGE was intragastrically injected for garlic group. Ten mg/kg of colistin was intraperitoneally injected for 6 consecutive days for colistin group. One percent of ABGE was done 30 min prior to colistin injection for treatment group. Rats were sacrificed on the next day after last colistin injection. Colistin injection increased the serum levels of blood urea nitrogen and creatinine; however, ABGE prevented deterioration of these serum levels. ABGE also alleviated tubular damage, including vacuolation and necrosis. TUNEL-positive cells were observed less frequently for the ABGE-treated groups. CD68 positive cells were significantly decreased by pretreatment with ABGE. Levels of oxidative stress biomarkers such as 8-hydroxydeoxyguanosine and malondialdehyde were lower in the ABGE-treated groups. Levels of NF-κB, inducible NO synthase, COX-2, and TGF-ß1 were lower in rats that had been treated with ABGE injection. Renal levels of IL-1ß and TNF-α were increased by colistin administration whereas renal SOD, catalase, and GSH levels were restored by ABGE administration. These results suggest that ABGE, which has antioxidant and anti-inflammatory properties, might be a potential therapeutic agent to prevent renal toxicity of colistin.

Urinothorax after ultrasonography-guided renal biopsy: a case report.

BACKGROUND: Urinothorax is defined as the presence of urine in the pleural space and is a rather rare cause of transudate pleural effusion. The potential etiologies are urinary tract obstruction and trauma. Diagnosis requires a high index of clinical suspicion and the condition is completely reversible following relief of underlying disease. CASE PRESENTATION: We report a 27-year-old man who developed urinothorax after renal biopsy. Urine leakage was confirmed with 99mTc DTPA (diethylenetriaminepentacetate) and single-photon emission computed tomography scans and retrograde pyelography. The pleural effusion was completely resolved by removing the leakage with a Foley catheter and a double J stent. CONCLUSIONS: Urinothorax has not been reported in patients doing renal biopsy in the literature. Based on our experience, urinothorax should be suspected, diagnosed, and managed appropriately when pleural effusion occurred after renal biopsy.

The logistic organ dysfunction system score predicts the prognosis of patients with alcoholic ketoacidosis.

Alcoholic ketoacidosis (AKA) is occasionally associated with multiple complications leading to death. However, no study has yet evaluated prognostic factors in patients with AKA. It is known that the logistic organ dysfunction system (LODS) score is an objective and useful index to predict the prognosis. We used LODS score to predict prognosis of AKA. We retrospectively reviewed the medical records of 46 patients who were diagnosed as AKA in our hospital. The mean LODS score was 6.3. The probability of mortality based on the LODS score was 36.6%, and 16 patients (34.5%) did, in fact, die. The total LODS score and lactate dehydrogenase (LDH) were significantly higher in the non-survival group. Prothrombin activity, serum platelet number, and the serum albumin levels were significantly higher in the survival group. We found significant correlations between the LODS score and arterial pH, the albumin level, and the LDH concentration. Multivariate analysis showed that the serum albumin and LDH levels were independently associated with survival in AKA patients. AKA patients suffered high-level mortality and the LODS score was an accurate predictor of prognosis. Clinicians may use the LODS score to this end.

The incidence, risk factors, and clinical outcomes of acute kidney injury (staged using the RIFLE classification) associated with intravenous acyclovir administration.

Intravenous (IV) acyclovir is commonly administered medication for viral infection but is well known for its nephrotoxicity. However, there was no study for incidence, risk factors, and clinical outcomes of acute kidney injury (AKI) associated with IV acyclovir administration. We retrospectively reviewed the medical records of 287 patients who were medicated IV acyclovir from January 2008 to May 2013 in Gyeongsang National University Hospital. All had documented medical histories and underwent medical review. Demographic data, risk factors, concomitant drugs, laboratory findings and outcome were gathered from the medical records and analyzed. AKI occurred in 51 patients (17.8%). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (62.7%), renal injury (15.6%), and renal failure (21.6%). There was no significant difference in age, sex, total dose, drug duration, and presence of hydration between AKI and non-AKI group. However, systolic pressure, underlying diabetes, concomitant vancomycin and non-steroidal anti-inflammatory drugs (NSAIDs) use was positively correlated with AKI occurrence (p = .04, p < .001, 0.01, and 0.04, respectively). Two patients underwent hemodialysis and these patients died. Higher mortality was observed in AKI patients (p < .001). Multivariate analysis also presented that presence of diabetes, concomitant NSAIDs, and vancomycin use was independent risk factor of acyclovir associated with AKI (p = .001, OR 3.611 (CI: 1.708-7.633), p = .050, OR 2.630 (CI: 1.000-6.917), and p = .009, OR 4.349 (CI: 1.452-13.022), respectively). AKI is relatively common in patients administrating acyclovir injection. Physicians should attempt to prevent, detect, and manage acyclovir associated AKI in patients prescribing acyclovir due to possible association of poor prognosis.

Association between colistin dose and development of nephrotoxicity.

OBJECTIVE: To investigate the development of nephrotoxicity associated with colistin dose, and whether this relationship differs depending on renal function. DESIGN: A retrospective cohort study of patients who received intravenous colistin to treat infections caused by extensively drug-resistant Gram-negative microorganisms. Adult patients receiving colistin for 72 hours or longer were included in this study. Patients who received renal replacement therapy at baseline or were administered colistin for less than 3 days were excluded. Colistin-induced nephrotoxicity was defined as a doubling of baseline serum creatinine. Colistin dosing was evaluated based on both actual body weight and ideal body weight. SETTING: Single general hospital between 2010 and 2013. PATIENTS: A total number of 475 patients received colistin therapy. Of these patients, 329 met the inclusion criteria and were included in the analysis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: One hundred forty-three patients (43.5%) experienced nephrotoxicity during colistin treatment. The median onset time of nephrotoxicity was 6 days (interquartile range, 4-8 days). The patients with nephrotoxicity were older. Hematocrit and serum albumin levels were lower in patients with nephrotoxicity. Median daily dosing of colistin based on ideal body weight was significantly higher in patients with nephrotoxicity than in those without nephrotoxicity (4.55 vs 4.43 mg/kg/d, respectively; p=0.021). The cumulative dose was not different between patients with and without nephrotoxicity. In multiple logistic regression analysis, daily colistin dosing based on ideal body weight was only significantly associated with the development of nephrotoxicity in patients with an estimated glomerular filtration rate<60 mL/min/1.73 m2 (odds ratio, 2.34; 95% CI, 1.22-4.5). In these affected patients, based on a receiver operating characteristic plot, the optimal predictive cutoff of colistin dose for the development of nephrotoxicity was 2.87 mg/kg/d of colistin, with a sensitivity of 92.3% and a specificity of 76.7%. In patients with estimated glomerular filtration rate≥60 mL/min/1.73 m, age, serum albumin, hematocrit, and use of glycopeptide were associated with the development of nephrotoxicity. CONCLUSIONS: Development of nephrotoxicity was significantly more strongly associated with the dose of colistin, but only in patients with an estimated glomerular filtration rate<60 mL/min/1.73 m2 and not in those with normal renal function.

Glutamine protects against cisplatin-induced nephrotoxicity by decreasing cisplatin accumulation.

Cisplatin is a chemotherapeutic drug but induces acute kidney injury (AKI). Cisplatin-induced AKI depends on several signaling pathways leading to apoptosis in tubular epithelial cells. Glutamine is a substrate for the synthesis of glutathione, the most abundant intracellular thiol and antioxidant, and plays an important role in protecting cells from apoptosis induced by different stimuli. In the present study, we investigated the protective effect of glutamine on cisplatin-induced AKI. Rats were divided into control, glutamine, cisplatin, and cisplatin plus glutamine groups. Glutamine ameliorated renal dysfunction, tissue injury, and cisplatin-induced apoptosis. Cisplatin increased cell death, caspase-3 cleavage, activation of MAPKs and p53, oxidative stress, and mRNA expression of TNF-α and TNFR1 in HK-2 cells. Glutamine treatment reduced cisplatin-induced these changes in HK-2 cells. Notably, glutamine reduced the cisplatin-induced expression of organic cation transporter 2 (OCT2) and cisplatin accumulation. Our results suggest that the protective effect of glutamine on cisplatin is specific for proximal tubular cells and the initial effects may be related to attenuation of cisplatin uptake. Thus, glutamine administration might represent a new strategy for the treatment of cisplatin-induced AKI.

The incidence, risk factors, and outcomes of acute kidney injury in patients with pyogenic liver abscesses.

BACKGROUND: Acute kidney injury (AKI) can occur in various infectious conditions. Liver abscess is relatively rare, but can lead to sepsis and/or other severe complications. Few studies of AKI in patients with a liver abscess have been conducted. Therefore, we analyzed the clinical and laboratory data of AKI in patients with a liver abscess. METHODS: We retrospectively reviewed the medical records of patients who were diagnosed with a liver abscess from January 2000 to March 2013. The study included 404 patients with a liver abscess confirmed by clinical presentation and computed tomography. RESULTS: AKI occurred in 137 patients (34 %). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (35.8 %), renal injury (47.4 %), and renal failure (16.5 %). AKI occurred more frequently in males and patients with liver cirrhosis (P < 0.001 and P = 0.005). Patients with AKI had lower serum albumin and higher AST and ALT levels than did patients without AKI. Bacteria were frequently isolated in AKI patients from blood culture and liver abscess aspirates (P < 0.001 and P = 0.007). The occurrence of septic shock was positively correlated with AKI (P = 0.002) and AKI was more frequent in patients with chronic kidney disease (P = 0.04). Higher mortality was observed in CKD patients accompanied by AKI (P < 0.001). Three patients with AKI underwent hemodialysis; two patients who had initially normal renal function completely recovered whereas one CKD patient progressed to ESRD, requiring maintenance hemodialysis. CONCLUSION: AKI is relatively common in patients with liver abscess. Physicians should therefore attempt to prevent, detect, and manage AKI early in patients with liver abscess.

Macrophage depletion ameliorates glycerol-induced acute kidney injury in mice.

BACKGROUND: This study was conducted to elucidate the role of renal macrophages in the development of acute kidney injury (AKI) in a glycerol (Gly)-induced rhabdomyolysis mouse model. METHODS: The experimental model of rhabdomyolysis requires injecting 50% Gly (10 ml/kg) intramuscularly into mice. Control mice were injected into the tail vein with the liposomal vehicle. Liposome-encapsulated clodronate (LEC)-only mice were injected with LEC. Gly-only mice were injected with Gly into a hind limb. LEC+Gly-treated mice were injected intravenously with 100 µl of LEC 24 h prior to Gly injection. Mice were sacrificed 24 h after Gly injection. RESULTS: Gly injection increased the serum creatinine level, and induced tubular damage. Renal CD45(+)CD11b(+)Ly6c(+) or CD45(+)CD11b(+)Ly6c(+)F4/80(+) macrophages were decreased by pretreatment with LEC in both normal and injured kidneys. Macrophage depletion prevented Gly-induced apoptotic death of tubular epithelial cells by decreasing caspase-9, ERK and p53, while increasing Bcl-2 expression. Expression of the inflammatory mediators NF-κB, MCP-1, ICAM-1, iNOS and COX-2 were also decreased with LEC pretreatment of mice injected with Gly. CONCLUSION: These results support the hypothesis that depletion of macrophages prevents renal dysfunction by abrogating apoptosis and attenuating inflammation during AKI.

Hemolytic uremic syndrome associated with paraquat intoxication.

We report a case of a 66-year-old patient with paraquat intoxication resulting in the requirement for hemoperfusion, hemodialysis, and plasma exchange. His initial serum paraquat level was 0.24 µg/mL (0.0-0.1 µg/mL). Activated charcoal (50 g) was administered orally, and high-dose N-acetylcysteine (150 mg/kg) was administered intravenously. In addition, immediate 4 h hemoperfusion was also performed for three consecutive days after admission. Hemodialysis was started on the 4th day after admission because of uremia. On the 9th day after admission, laboratory findings demonstrated hemolytic uremic syndrome (HUS): microangiopathic hemolytic anemia (MAHA), thrombocytopenia, elevated reticulocyte count, and lactate dehydrogenase (LDH). Plasma exchange was performed three times consecutively. Anemia and thrombocytopenia were improved, and LDH was normalized after plasma exchange. Urine output increased to 2240 mL/day on the 18th day after admission, and hemodialysis was discontinued. He is currently being observed at our follow-up clinic without renal impairment or pulmonary dysfunction for 1.5 years since discharge. We should suspect paraquat-associated HUS when thrombocytopenia and anemia are maintained for a long time after paraquat intoxication.

Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace.

A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8 mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3 = 130.40 ng/dL, TSH = 0.06 mIU/L, and free T4 = 1.73 ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4 mmol/L by intravenous infusion of only 40 mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient's thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea.

A retrospective study of short- and long-term effects on renal function after acute renal infarction.

PURPOSE: Acute renal infarction is often missed or diagnosed late due to its rarity and non-specific clinical manifestations. This study analyzed the clinical and laboratory findings of patients diagnosed with renal infarction to determine whether it affects short- or long-term renal prognosis. METHODS: We retrospectively reviewed the medical records of 100 patients diagnosed as acute renal infarction from January 1995 to September 2012 at Gyeongsang National University Hospital, Jinju, South Korea. RESULTS: Acute kidney injury (AKI) occurred in 30 patients. Infarct size was positively correlated with the occurrence of AKI (p = 0.004). Compared with non-AKI patients, AKI occurrence was significantly correlated with degree of proteinuria (p < 0.001) and the presence of microscopic hematuria (p = 0.035). AKI patients had higher levels of aspartate transaminase (p < 0.001), alanine transaminase (p < 0.001), and lactated dehydrogenase (p = 0.027). AKI after acute renal infarction was more common in patients with chronic renal failure (CRF) (eGFR < 60 mL/min), compared with non-CRF patients, whose baseline eGFR was >60 mL/min (p = 0.003). Most patients recovered from AKI, except for seven patients (7%) who developed persistent renal impairment (chronic kidney disease progression) closely correlated with magnitude of infarct size (p = 0.015). Six AKI patients died due to combined comorbidity. CONCLUSIONS: AKI is often associated with acute renal infarction. Although most AKI recovers spontaneously, renal impairment following acute renal infarction can persist. Thus, early diagnosis and intervention are needed to preserve renal function.

Xanthogranulomatous pyelonephritis in a patient with polycystic kidney disease without underlying risk factors: a case report.

Xanthogranulomatous pyelonephritis (XGP) is an extremely rare, chronic granulomatous inflammatory condition thought to arise secondary to a combination of obstruction, recurrent bacterial infection and an incomplete immune response although the etiology of XGP is more complex. We would like to report a case of XGP occurring in a patient with polycystic kidney disease (PCKD), which has not been previously documented in etiology. A 29-year-old woman presented to our hospital with right upper quadrant pain for 5 days. She had experienced a low-grade fever, generalized weakness, and myalgia throughout her body for 2 weeks. She had no history of renal stones or recurrent UTIs. Contrast-enhanced CT revealed a well-enhancing large septated cystic mass in the right kidney and numerous cysts in the liver and both kidneys. Open right radical nephrectomy was performed due to the suspicion of renal cell carcinoma, as there was no response to antibiotics over 7 days. Gross specimen demonstrated architectural distortion due to xanthomatous nodules and a dilated pelvico-calyceal system filled with pus and blood. Microscopic examination revealed infiltration of neutrophils and lipid-laden macrophages. The patient is currently being followed up in the outpatient clinic without recurrence of XGP. This is the first reported case of XGP in a patient with underlying PCKD. Physicians should consider PCKD as a potential underlying cause of XGP.