Elevated Serum Creatinine Research Articles

#2334 Elevated serum admission creatinine in acute heart failure hospitalizations: lifting the veil to understand outcome differences

Abstract Background and Aims Organ crosstalk in heart failure and kidney dysfunction is prevalent and is associated to a high event rate. In this setting elevated serum creatinine (sCr) at acute decompensated heart failure (ADHF) admissions is a strong risk factor for poor outcomes. Current accepted cardiorenal syndrome (CRS) classification is based on timing and initial organ dysfunction and fails at capturing its nature and prognosis. We sought to describe patient (P) profile and outcomes in P hospitalized for ADHF with high admission sCr in function of current CRS classification and assess for stratifying predictors. Method We conducted an observational, analytical and cross-sectional study, with prospective and consecutive data acquisition. We included P over 18 years-old, who were admitted to the Intensive Care Telemetry Unit in our Hospital between July, 2011 and Dec, 2023 due to ADHF. P who received a heart transplant during index admission or those on chronic dialysis were excluded. Clinical, epidemiological and biochemical variables were registered. Renal dysfunction was defined under admission sCr >1.4 mg/dl and divided according to Ronco et al classification, as initially cardiac (type 2) or renal (type 4) origin. We constructed multivariate logistic and survival regression models, with selection of relevant predictors by resampling and regularization of a Lasso regression model. Statistical significance was considered with a 5% of alpha error level. Analysis was conducted using R (R Core Team, 2023). Results A total of 1868 consecutive P were included. P population consisted in type 2: 124 and type 4: 258 P, respectively. We found no differences in gender (p = 0.47), while type 4 were older (75 ± 12 vs 71 ± 12; p < 0.01). Ventricular dysfunction was more severe in type 2 (left ventricular ejection fraction 34 ± 17 vs 41 ± 16%; p < 0.001). While ischaemic heart disease was more prevalent in type 4 (32.8 vs 23.5%; p = 0.001), idiopathic cardiomyopathy was more frequent in type 2 (18.8 vs 7.2%; p = 0.001). Clinical phenotypes differed between groups, being clinical hypoperfusion more frequent in type 2 (32.4 vs 12.3%; p < 0.001). Admission sCr was higher in type 4 (1.9 [0.8] vs 1.6 [0.58] mg/dl; p < 0.001), as was 1st day natriuresis (81 vs 67 mEq; p = 0.01). Both groups experienced a similar diuretic resistance rate (21.2 vs 17.1%; p = 0.34), while type 4 received rescue ultrafiltration more frequently (11.3 vs 3.5%; p < 0.01). Type 2 received a higher inotropic support rate (47.1 vs 19.5%; p < 0.01) and had a longer length of stay (9 vs 7 days; p = 0.01). In-hospital (11.8 vs 11.3%; p = 0.99); 6-month and 1-year mortality rates (66.8 vs 72.8% and 55.1 vs 64.6% respectively; p = 0.3). In a similar way, 1-month (94.8 vs 94.7%), 6-month (72 vs 74.7%) and 1-year readmission rates (59.2 vs 60.9%; p = 0.6) were similar in both groups. A multiple logistic regression model (AUCROC 0.82) identified admission sCr (OR 2.6; CI 95% 2.2-3.2; p < 0.001), inotropic need (OR 1.87; CI 95% 1.4-2.6; p < 0.001), anasarca phenotype (OR 1.63; CI 95% 1.06-2.5; p = 0.02), moderate to severe right ventricular dysfunction (OR 1.4; CI 95% 1.03-1.9; p = 0.03) as independent predictors for a descending sCr behavior during hospitalization, while the lower T3 levels were associated with less probability for a descent of sCr (OR 0.21; CI 95% 0.1-0.46; p < 0.001). Conclusion Organ crosstalk in ADHF hospitalizations was associated with a high event rate. One-year mortality and readmission rates were similar in both groups. Renal support therapies were more frequent under lower kidney reserve conditions. Ventricular dysfunction and systemic congestion phenotype are relevant to a better understanding for potential reversibility at the admission time and may promote actions for outcome enhancing.

#1061 Brucella infection in a patient with renal cystic disease and renal imaging changes before and after treatment: a case report

Abstract Background and Aims Brucellosis can affect nearly all systems. Genitourinary involvement is uncommon in patients with brucellosis, accounting for approximately 10% of cases. We diagnosed a rare case of renal cysts with brucellosis and reported renal imaging changes before and after treatment. Method A 38-year-old man was admitted to our hospital in September 2021 with complaints of elevated serum creatinine, proteinuria for more than 2 months, and intermittent fever for 2 weeks. In July 2020, the patient experienced fatigue, and a rash on all four extremities. He denied experiencing low back pain or joint swelling. Urine analysis revealed the following: BLD (+), Pro (+), 24-hour urine protein (24 h UP) 0.7 g; blood: Cr 11.88 mg/dL, UA 77.51 mg/dL, ALP 217 IU/L, and GGT 227 IU/L. MRI revealed multiple small punctate areas with short T1 signals in both kidneys and splenomegaly. Soon, he experienced persistent afternoon fever with a maximum temperature of 39.0°C, along with night sweats and left lumbar pain. There were no symptoms of cough, expectoration, or urinary tract irritation. The patient had diabetes mellitus and diabetic retinopathy. He has lived in the Inner Mongolia Autonomous Region. He denied having any contact with raw milk or mice. His father and sister had kidney disease and diabetes. In September 2021, the patient was admitted to our hospital. Urinalysis revealed BLD (-), Pro 0.3 g/L, and 24 hUP 1.39 g; blood: HGB 117 g/L, ALP 227 U/L, GGT 221 U/L, Cr 2.56 mg/dL, UA 88.79 mg/dL, and K 3.2 mEq/L. The infection indicators were as follows: the standard tube agglutination test (+) (Fig. 1), Brucella (+) in blood culture, a positive qualitative test for blood cryptococcal antigen and qualitative positive results for 6 Cryptococcus neoformans sequences in bronchoalveolar lavage fluid using next-generation sequencing. Ultrasound showed multiple cysts in both kidneys. It also showed uneven echogenicity in the left testis and visible lymph nodes in the left neck, bilateral axillae and groin. CT revealed cavitary nodules and ground-glass opacities in the right middle lobe, as well as splenomegaly. MRI revealed renal cysts (Fig. 2a, b, c) and abscesses (Fig. 2e, f, g). The patient was diagnosed with stage 3 chronic kidney disease (CKD), pulmonary cryptococcosis, and brucellosis associated with renal abscess, left orchitis, splenomegaly, multiple lymphadenopathies, rash, and hyperuricemia. Doxycycline, rifampicin, and fluconazole were administered. He had no fever, his low back pain had disappeared, and his rash were relieved. Results A reexamination after 2 months revealed the following: the urinalysis results revealed a BLD (-), Pro(-), and 24 hUP 0.15 g; blood: GGT 107 IU/L; ALP 72 IU/L; Cr 1.89 mg/dL; UA 0.22 mg/dL; and K 4.0 mEq/L. Ultrasound revealed a decrease in the size of the spleen. MRI revealed the liquefaction of renal abscesses. Brucella therapy has been found to be effective. Conclusion The patient was a young man who was infected with both Brucella and Cryptococcus. Although his hometown was in an area affected by an epidemic, his current residence was not affected. Namely, he was immunocompromised, which was associated with diabetes. After receiving anti-Brucella treatment, his symptoms disappeared, the renal abscess liquefied, but creatinine decreased to levels similar to those at onset without a decreasing trend. These findings suggest that the patient had underlying CKD that was not associated with Brucellosis. We believe that the CKD was diabetes and renal cysts. He had hyperuricemia, hypomagnesaemia, unexplained asymptomatic abnormal liver function, and mild proteinuria. Imaging indicated the presence of renal cysts. In addition to having diabetes, he had a family history of kidney disease and diabetes. We diagnosed the patient with CKD and as having autosomal dominant tubulointerstitial disease (ADTKD) associated with the HNF1B pathogenic gene mutation. This gene mutation is also rare in ADTKD patients. Genetic testing revealed that the causative genes include NM001303448. Potential causative genes included NM000128. The mutated genes mentioned above are not typical causative genes for HNF1B or other types of ADTKD.

Acute kidney tubular injury after ingestion of red yeast rice supplement

ABSTRACT A 47-year-old woman developed severe kidney dysfunction after taking a lipid-lowering supplement, Red Yeast Rice Cholestehelp, for approximately 7 months. The patient developed sudden nausea and had an elevated serum creatinine level of 4.26 mg/dL. A kidney biopsy showed findings consistent with acute tubular necrosis. Kidney dysfunction improved with discontinuation of supplementation, and corticosteroid therapy. Similar kidney involvement has been reported, raising concerns regarding supplements in Japan. An investigation of the nephrotoxic ingredients in the same product batches is currently underway. This report underscores the need for public awareness and warnings of health risk concerns associated with unregulated supplements.

Association of Tumor Necrosis Factor-Alpha (TNF-α) rs1800629 Polymorphism in Chronic Kidney Disease.

Background Chronic kidney disease (CKD) is characterized by progressive loss of kidney function. Tumor necrosis factor-alpha (TNF-α) is a cytokine implicated in inflammatory processes, including those affecting the kidneys. Although this association is not yet comprehensible, a tie-up between renal disease and markers of inflammation - interleukin-6 (IL-6), preceded by TNF-α - is eminent. However, a pause in research is evident concerning the TNF-α gene with kidney disease in the inhabitants of India. So, this study investigates the association between TNF-α rs1800629 polymorphism and CKD. Methodology A prospective case-control study was conducted in Andhra Pradesh for over three years. A total of 579 patients participated in the study. These were divided into premature, late-stage CKD, and control groups. The amplification refractory mutation system (ARMS)-polymerase chain reaction (PCR)was used, and biochemical investigations and genotyping were carried out for the study participants. Hardy-Weinberg expected frequencies (HWE) with chi-square test was used for detecting allele and genotype frequencies. The association between TNF-α (-308 G/A, rs1800629) and CKD was assessed using odds ratios (ORs) with 95% confidence intervals (CIs). Results We found a higher prevalence of CKD among males (n= 301, 52%) compared to females (n= 278, 48%).Both male and female participants diagnosed with CKD exhibited significantly elevated blood urea and serum creatinine levels compared to the control group, indicating impaired kidney function.Furthermore, these markers were generally higher in the late-stage CKD group compared to the early-stage group, suggesting a progressive decline in kidney function as the disease worsens. The homozygous genotype GG was more prevalent in late-stage CKD patients compared to both early-stage CKD patients and controls. Further, the heterozygous genotype GA was more frequent in the early-stage CKD group compared to the late-stage group.The homozygous genotype AA also showed a higher prevalence in the early-stage CKD group compared to the late-stage group. The G/G genotype and the G allele (rs1800629) were significantly associated with susceptibility to CKD (P<0.005). Conclusions Our study reported the TNF-α rs1800629 polymorphism and CKD risk in a South Indian population. G/G genotype and the G allele (rs1800629) were significantly associated with the risk of CKD. However, further research with larger sample sizes is warranted to confirm these observations and elucidate the underlying mechanisms by which TNF-α might influence CKD risk.

Comparison of serum SDMA and creatinine as a biomarker for the detection of meloxicam-induced kidney injury in cats.

Serum symmetric dimethylarginine (SDMA) and creatinine are commonly used biomarkers of renal function in cats. We hypothesize that the serum analytes creatinine and SDMA are equally effective at detecting impaired renal function caused by meloxicam-induced renal injury in cats. Our primary objective was to compare serum concentrations of SDMA and creatinine in cats before, during, and after induction of renal injury from repeated dosages of meloxicam in the context of a small pilot study. This follow-up study results from data collected in a well-controlled study that included 12 healthy female adult purpose-bred cats. Cats in the treatment group received meloxicam 0.3 mg/kg subcutaneously (SC) every 24 h for 31 days. Cats in the control group received saline (0.1 mL SC). Renal injury was defined as the presence of tubular damage, basement membrane damage, and/or interstitial inflammation in histological sections of kidney tissue. Serum creatinine and SDMA concentration were measured every 4 days. In the control group, no cats developed renal azotemia. In the treatment group, four out of six cats developed elevated serum creatinine and histopathological evidence of renal injury. Three of these cats developed an elevation in serum SDMA. The time to the development of renal azotemia using serum creatinine or SDMA was not significantly different (p > 0.05). In this pilot study, there was no evidence that serum SDMA was superior to serum creatinine at detecting impaired renal function caused by meloxicam-induced renal injury in cats.

Renoprotective effect of Nesfatin-1 in Adenine-Induced Chronic kidney Disease: An in vitro and in vivo study

Chronic Kidney Disease (CKD) presents a significant global health challenge with limited treatment options. Nesfatin-1, an anorexigenic peptide, has demonstrated antioxidant, anti-inflammatory, and anti-apoptotic properties in various diseases. However, the role of nesfatin-1 in CKD remains unclear. This study investigates the potential renoprotective effects of nesfatin-1 in adenine-induced CKD mice and in NRK-52E renal epithelial cells.Male C57BL/6J mice and NRK-52E renal epithelial cells were administered adenine to induce CKD. Various aspects of renal function, histopathology, oxidative stress, inflammation, apoptosis, and renal interstitial fibrosis were assessed and downstream pathways were investigated.Adenine-fed mice exhibited reduced nesfatin-1 expression and increased markers of kidney damage, including elevated blood urea nitrogen (BUN), serum creatinine, and histological abnormalities, reactive oxygen species (ROS), inflammation, apoptosis, and fibrosis. Treatment with nesfatin-1 in adenine induced mice significantly reversed these changes. Nesfatin-1 also lowered calcium levels and the expression of inflammatory markers, including IL-1β, IL-6, TNF-α, and Nf-kB. Furthermore, nesfatin-1 reduced the expression of apoptotic markers (Caspase-3, Caspase-1, Bax/Bcl2 ratio) and restored the balance of Bcl2 and MMP. Lastly, nesfatin-1 attenuated fibrotic markers (Tgf-β, Smad2/3,4, type IV collagen, α-SMA) in both adenine-induced CKD mice and NRK-52E cells.In conclusion, our results suggest that nesfatin-1 may enhance kidney function in adenine-induced CKD mice and NRK-52E cells. The renoprotective effects of nesfatin-1 are likely associated with its antioxidant, anti-inflammatory, anti-apoptotic, and anti-fibrotic properties.

Cancer drugs and acute kidney injury: new therapies and new challenges.

Cancer therapies continue to evolve at a rapid pace and although novel treatments, including immunotherapies and targeted therapies have allowed for substantial improvements in cancer survival, they carry associated risks of acute kidney injury (AKI). We aim to summarize the existing literature on AKI associated with the spectrum of systemic cancer treatments, including conventional chemotherapies, newer immunotherapies, and the growing number of targeted cancer therapies, which may be associated with both AKI and 'pseudo-AKI'. Conventional cytotoxic chemotherapies (e.g. cisplatin and other platinum-based agents, methotrexate, pemetrexed, ifosfamide, etc.) with well recognized nephrotoxicities (predominantly tubulointerstitial injury) remain in widespread use. Immunotherapies (e.g., immune checkpoint inhibitors and CAR-T therapies) may be associated with kidney immune-related adverse events, most often acute interstitial nephritis, and rarely, glomerular disease. Recently, multiple targeted cancer therapies have been associated with reduced renal tubular secretion of creatinine, causing elevations in serum creatinine and apparent 'pseudo-AKI'. To complicate matters further, these agents have had biopsy-proven, 'true' kidney injury attributed to them in numerous case reports. Clinicians in nephrology and oncology must be aware of the various potential kidney risks with these agents and recognize those with clinically meaningful impact on both cancer and kidney outcomes.

Immune checkpoint inhibitors induce acute interstitial nephritis in mice with increased urinary MCP1 and PD-1 glomerular expression

IntroductionImmune checkpoint inhibitors (ICIs) induce acute interstitial nephritis (AIN) in 2–5% of patients, with a clearly higher incidence when they are combined with platinum derivatives. Unfortunately, suitable disease models and non-invasive biomarkers are lacking. To fill this gap in our understanding, we investigated the renal effects of cisplatin and anti-PD-L1 antibodies in mice, assessing PD-1 renal expression and cytokine levels in mice with AIN, and then we compared these findings with those in AIN-diagnosed cancer patients.MethodsTwenty C57BL6J mice received 200 µg of anti-PD-L1 antibody and 5 mg/kg cisplatin intraperitoneally and were compared with those receiving cisplatin (n = 6), anti-PD-L1 (n = 7), or saline (n = 6). After 7 days, the mice were euthanized. Serum and urinary concentrations of TNFα, CXCL10, IL-6, and MCP-1 were measured by Luminex. The kidney sections were stained to determine PD-1 tissue expression. Thirty-nine cancer patients with AKI were enrolled (AIN n = 33, acute tubular necrosis (ATN) n = 6), urine MCP-1 (uMCP-1) was measured, and kidney sections were stained to assess PD-1 expression.ResultsCisplatin and anti PD-L1 treatment led to 40% AIN development (p = 0.03) in mice, accompanied by elevated serum creatinine and uMCP1. AIN-diagnosed cancer patients also had higher uMCP1 levels than ATN-diagnosed patients, confirming our previous findings. Mice with AIN exhibited interstitial PD-1 staining and stronger glomerular PD-1 expression, especially with combination treatment. Conversely, human AIN patients only showed interstitial PD-1 positivity.ConclusionsOnly mice receiving cisplatin and anti-PDL1 concomitantly developed AIN, accompanied with a more severe kidney injury. AIN induced by this drug combination was linked to elevated uMCP1, consistently with human AIN, suggesting that uMCP1 can be potentially used as an AIN biomarker.

A Systematic Review of Perinuclear Antineutrophil Cytoplasmic Antibody-Associated Glomerulonephritis Following Coronavirus Disease 2019 Vaccination: A 2024 Update.

Antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (GN) is an immune-mediated kidney disease characterized by the inflammation of small blood vessels in the kidney, leading to renal impairment and potentially irreversible damage. Concerns have been raised over the reports of myeloperoxidase/perinuclear (MPO/p) ANCA GN following the coronavirus disease 2019 (COVID-19) vaccination. Our study provides a comprehensive insight into perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) GN after COVID-19 vaccination. We conducted a comprehensive literature search on PubMed, Cochrane Library, and EMBASE using the Medical Subject Headings (MeSH) terms related to "covid-19 vaccine," "glomerulonephritis," "p-ANCA," and "MPO-ANCA" up to March 5, 2024, to include cases of p-ANCA-associated GN following COVID-19 vaccination. Of the 4,102 articles, we included 29, reporting 35 patients demonstrating COVID-19 vaccine-induced p-ANCA GN, with 23 (65.7%) females and a median age of 69 years (mean ± SD = 63.22 ± 16). Twenty-six (74.28%) patients received the mRNA vaccine (Pfizer = 19, Moderna = 7). Seventeen (48.57%) patients presented with p-ANCA GN after the second dose of the COVID-19 vaccine, with a median gap of 19 days (1-84 days). Constitutional symptoms (54.28%) and acute kidney injury (42.85%) were the most reported initial presentations, and elevated serum creatinine (mean peak serum creatinine = 4.98 ± 5.02 mg/dL), hematuria, and proteinuria were the laboratory findings. MPO/p-ANCA was positive in 31 (88.6%) patients. All patients underwent renal biopsy, and crescentic GN was the most common finding among 27 (77.14%) patients. Management of p-ANCA GN included steroids in 30 (85.71%) patients, followed by rituximab (28.57%), and plasmapheresis (22.86%). Most patients responded well to treatment, with complete remission in 29 (82.86%) and relapse in four (11.42%) patients. Two patients did not achieve remission and became dialysis dependent. ANCA-associated GN is a rare and life-threatening complication of the COVID-19 vaccine, necessitating urgent evaluation and management. COVID-19 vaccine-induced p-ANCA GN should be included in the differential diagnoses of patients presenting with kidney injury after vaccination.

Role of cAMP/pCREB and GSK-3β/NF-κB p65 signaling pathways in the renoprotective effect of mirabegron against renal ischemia-reperfusion injury in rats

Acute kidney injury and other renal disorders are thought to be primarily caused by renal ischemia-reperfusion (RIR). Cyclic adenosine monophosphate (cAMP) has plenty of physiological pleiotropic effects and preserves tissue integrity and functions. This research aimed to examine the potential protective effects of the β3-adrenergic receptors agonist mirabegron in a rat model of RIR and its underlying mechanisms. Male rats enrolled in this work were given an oral dose of 30 mg/kg mirabegron for two days before surgical induction of RIR. Renal levels of kidney injury molecule-1 (KIM-1), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), Interleukin-10 (IL-10), cAMP, cAMP-responsive element binding protein (pCREB), and glycogen synthase kinase-3 beta (GSK-3β) were assessed along with blood urea nitrogen and serum creatinine. Additionally, caspase-3 and nuclear factor-kappa B (NF-κB) p65 were explored by immunohistochemical analysis. Renal specimens were inspected for histopathological changes. RIR led to renal tissue damage with elevated blood urea nitrogen and serum creatinine levels. The renal KIM-1, MCP-1, TNF-α, and GSK-3β were significantly increased, while IL-10, cAMP, and pCREB levels were reduced. Moreover, upregulation of caspase-3 and NF-κB p65 protein expression was seen in RIR rats. Mirabegron significantly reduced kidney dysfunction, histological abnormalities, inflammation, and apoptosis in the rat renal tissues. Mechanistically, mirabegron mediated these effects via modulation of cAMP/pCREB and GSK-3β/NF-κB p65 signaling pathways. Mirabegron administration could protect renal tissue and maintain renal function against RIR.

Moringa oleifera-based feed supplement protects against renal ischaemia/reperfusion injury via downregulation of Bax/caspase 3 signaling.

Ischaemia/reperfusion (I/R) may lead to acute kidney injury via the induction of oxidative stress. On the other hand, Moringa oleifera has been reported to exert antioxidant activities. This study was designed to assess whether or not Moringa oleifera-based feed supplement could prevent I/R-induced renal injury. Renal I/R was induced by occluding the right renal artery for 30 min followed by a 2-h reperfusion. Renal I/R led to increased absolute renal weight and renal organo-somatic weight index. Renal I/R also caused distortion of renal histoarchitecture and impaired renal function evidenced by elevated serum creatinine and blood urea nitrogen. In addition, renal I/R significantly elevated renal levels of hydrogen peroxide, MDA, and advanced oxidation protein products, but suppressed the levels of reduced glutathione, protein thiol, and non-protein thiol, and the activities of superoxide dismutase and glutathione peroxidase. In addition, renal I/R up-regulated myeloperoxidase activity and the renal levels of NO, TNF-α, and IL-6. Renal I/R also up-regulated Bax and caspase 3 expression in the kidney. Furthermore, I/R-driven structural and biochemical alterations were markedly inhibited by Moringa oleifera-based feed supplement. These results suggest that Moringa oleifera-based feed supplement may preserve the gross and histoarchitectural integrity of the kidney as well as renal function via downregulation of Bax/caspase 3 signaling by targeting oxidative stress, inflammation and apoptosis in the kidney of I/R rat.

Predictive factors of developing lupus nephritis in systemic lupus erythematosus

Renal involvement is common in systemic lupus erythematosus (SLE), and even without elevated serum creatinine, there is a high proportion of abnormal urine analysis in these patients. Lupus nephritis (LN) develops early in the course of the disease in 50% of SLE patients, and end stage renal disease (ESRD) occurs in 4.3-10.1%. We performed a keyword-based literature search and included 31 articles published from 2004 to 2023. Ethnic and racial differences may affect LN, including higher incidence of LN in Black, Hispanic and Asian compared with white patients. In addition, male sex, longer disease duration, smoking, low albumin globulin ratio, low complement, anti-double stranded DNA, high anti-Sm is associated with disease progression to LN. High serum creatinine (&gt;1.5 mg/dL) at disease onset is the most commonly reported independent clinical laboratory predictor for ESRD in patients with SLE. Other factors indicating an increased risk for ESRD are higher chronicity index, high systolic blood pressure, black race, male sex, hypocomplementemia, class of LN (III, IV and V) and older age.

Tumor lysis syndrome in induction therapy for acute myeloid leukemia before the rasburicase era.

Guidelines recommend rasburicase for high-risk patients to prevent tumor lysis syndrome (TLS). However, little information is available on the incidence and outcome of TLS in AML patients. We analyzed 145 patients with AML who underwent induction therapy before the approval of rasburicase to evaluate the incidence of TLS and the necessity of rasburicase as prophylaxis. Three patients had already developed clinical TLS (CTLS) at diagnosis of AML, and another three developed CTLS after the initiation of chemotherapy. In patients without TLS at diagnosis of AML, the risk for developing TLS was classified as high in 44 patients, intermediate in 41 and low in 57, according to the current guidelines. Allopurinol alone was administered to prevent hyperuricemia in all patients. All three patients who developed CTLS after diagnosis of AML were at high risk of TLS, and had elevated serum creatinine levels and a WBC count greater than 200,000 per microliter at diagnosis of AML. Allopurinol may be insufficient to prevent TLS in high-risk patients with renal dysfunction at diagnosis of AML, especially those with a high tumor burden and a WBC count of 200,000 or more, which indicates that prophylactic administration of rasburicase should be considered.

Magnesium supplementation therapy to prevent cisplatin-induced acute nephrotoxicity in pediatric cancer: a randomized phase-2 trial.

The present study aimed to examine the effect of magnesium (Mg) supplementation on cisplatin-induced nephrotoxicity (CIN) in pediatric cancer patients. The present phase-2, open-label, multicenter, randomized controlled trial enrolled patients aged less than 20years who were scheduled to receive cisplatin-containing chemotherapy and randomly allocated them at a ratio of 1:1 to a Mg supplementation arm with even-numbered chemotherapy courses (arm AB) or another arm with odd-numbered courses (arm BA). Analysis objects were reconstructed into two groups depending on whether the chemotherapy course had Mg supplementation (group B) or not (group A). The primary outcome was the proportion of chemotherapy courses resulting in elevated serum creatinine per chemotherapy course. The secondary outcomes included efficacies evaluated using other biomarkers and the safety of the Mg supplementation. Twenty-eight patients were randomly allocated to either group (16 to arm AB and 12 to arm BA). The baseline characteristics of the groups were similar. There was no significant difference in the proportion of courses with increased serum creatinine between the groups (group A: 10% vs. group B: 6%; P = 0.465) nor was any significant difference observed in other biomarkers during any chemotherapy course. The Mg value during chemotherapy was significantly higher in group B than that in group A. No adverse events related to magnesium administration were observed. The study design, which treated a single chemotherapy course as a study object, failed to detect a statistically significant benefit of Mg supplementation for preventing CIN in pediatric cancer patients. JRCT ( https://jrct.niph.go.jp/ ) Identifier UMIN000029215 jRCTs031180251. UMIN-CTR ( http://www.umin.ac.jp/icdr/index.html ) Identifier UMIN000029215.

Plasmodium Falciparum associated Rhabdomyolysis

Rhabdomyolysis-induced acute kidney injury (AKI) is highly unusual in P. falciparum-infected patients. Only a handful of cases have been described in the form of case reports, and the clear pathophysiology behind malaria producing the rhabdomyolysis is unclear. A 55-year-old man with a past medical history of 12 years of alcohol abuse presented to the Emergency Department with a 5-day history of on and off fevers and a 1-day history of pain in the abdomen, vomiting, and shortness of breath. Following initial investigations, the patient was found positive for Plasmodium falciparum infection. The patient was treated with intravenous (IV) artesunate, and on day-2 of admission, the patient developed anuria, severe respiratory distress, and bradycardia and had to be intubated and upgraded to intensive level care; further evaluation revealed elevated serum creatinine and myoglobinuria and diagnosis of secondary rhabdomyolysis and AKI. He was managed with forced alkaline diuresis, and a urine output higher than 200ml/hour was maintained with IV fluids. The patient consequently also developed symptoms of alcohol withdrawal, and lorazepam was added for management. On days 5-6 of admission, his symptoms started to improve, and his serum markers of rhabdomyolysis and AKI normalized. The patient was extubated, discharged, remains in follow-up, and has no residual sequelae due to this episode of illness.

A CASE STUDY ON AYURVEDIC MANAGEMENT OF CHRONIC KIDNEY DISEASE

Chronic kidney disease (CKD) is a progressive and irreversible condition that ranks among the leading causes of mortality worldwide. Its development is often linked to hypertension and diabetes, which gradually lead to renal impairment progressing to CKD and potentially to end-stage renal disease. Traditional treatments for CKD, such as dialysis and renal replacement therapy, are financially burdensome for many patients, highlighting the need for alternative, more affordable, and safe approaches. In Ayurveda, CKD is addressed under the concept of mutravah srotas vikar, and also mutrakshaya will be seen which is a main symtpom seen in mutraghata. Seeking an alternative to hemodialysis, a 55-year-old male patient from New Delhi visited the Outpatient Department (OPD) of Kayachikitsa for an Ayurvedic intervention. The treatment approach involved the administration of shamanaushadhi to reduce elevated serum creatinine and blood urea levels. Specific Ayurvedic medications known for their nephroprotective and diuretic properties were prescribed, including Renogrit, Gokshuradi guggulu, Chandraprabha vati, and Punarnavadi madoor. These herbal formulations are believed to exert beneficial effects on kidney function. The holistic Ayurvedic approach aimed to alleviate symptoms, slow down CKD progression, and potentially circumvent the need for hemodialysis. By addressing underlying imbalances and supporting kidney health, Ayurvedic treatment offers a promising alternative for CKD management.

A Study Assessing the Role of Renal Grayscale Ultrasonography and Flowmetry in Correlation With Renal Function Tests Across Various Renal Diseases.

Background Renal insufficiency, a critical concern in native and transplant kidneys, necessitates effective screening modalities for evaluation and management. Grayscale sonography has been a cornerstone in renal diagnostics, providing basic anatomical insights such as renal length, cortical thickness, and collecting system dilatation. Despite technological advancements, its impact on the differential diagnosis or management of renal disease remains limited, often showing normal findings in the presence of severe renal dysfunction. On the other hand, Doppler sonography, particularly the Doppler resistive index (RI), has shown potential in enhancing the assessment of renal dysfunction by quantifying alterations in renal blood flow and correlating with various renal pathologies and prognoses. Thus, this study aims to assess and compare the sensitivity of transabdominal and Doppler sonography as a diagnostic modality to evaluate medical renal diseases with altered renal function tests (RFTs). Methodology Participants included patients visiting the ultrasonography (USG)room at our hospital for USG of the kidneys, ureters, and bladder (USG KUB) and USG of the whole abdomen(USG W/A) with altered RFTs. Each underwent renal grayscale USG and RImeasurement, alongside standard RFTs, aiming to investigate the relationship between USG and RI findings and RFT outcomes to assess their predictive accuracy for renal function. Renal grayscale USG assessed parameters including renal dimensions, echogenicity, corticomedullary differentiation, and RI. Data management and charting were conducted with Microsoft Excel 2021 and Microsoft Word 2021. IBM SPSS Statistics for Windows, Version 24 (IBM Corp.,Armonk, NY) was utilized for data analysis. The analysis of variance (ANOVA) test examined relationships between renal parameters and RI across diagnostic groups. Furthermore, the chi-square test evaluated associations of renal ultrasound findings with RFTs and their significance. Results The study analyzed 93 patients with altered RFTs. Chronic kidney disease (CKD) affected 68 patients, primarily males in their fifth and sixth decades, showing reduced renal dimensions, increased cortical echogenicity, and elevated Doppler RI mean (RIm) with 83% sensitivity. Acute kidney injury (AKI) was found in 12 patients, mainly in their fourth decade, displaying increased renal parameters and elevated RIm with 75% sensitivity. Glomerular diseases, including nephrotic syndrome (NS) and nephritic syndrome (NeS), occurred in 9 patients, predominantly males in their fourth decade, with heightened renal cortical echogenicity and elevated RIm with 55.5% sensitivity. Lupus nephritis (LN) was detected in 4 female patients, despite normal renal parameters, showing elevated serum creatinine levels. Conclusions Doppler assessment of renal vascular waveforms effectively identifies chronic renal changes, aiding in the diagnosis of altered RFTs and guiding prognosis. While it detects typical changes like decreased size and parenchymal atrophy, it may not be as indicative of diabetic nephropathy. Key ultrasound indicators such as changes in echotexture and size, along with associated findings like ascites and effusions, help recognize altered renal function and minimize unnecessary interventions.

Short-Term Mortality in Hospitalized Patients with Congestive Heart Failure: Markers of Thrombo-Inflammation Are Independent Risk Factors and Only Weakly Associated with Renal Insufficiency and Co-Morbidity Burden.

Congestive heart failure (CHF) is associated with significant morbidity and mortality. There has been renewed interest in using thrombo-inflammatory markers as prognostic tools in patients with CHF. To determine if thrombo-inflammatory markers are independent risk factors for 28-day mortality in hospitalized CHF patients, we retrospectively analyzed admission data extracted from 2008 consecutive patients admitted with a diagnosis of CHF to Zigong Fourth People's Hospital. Multivariate Cox proportional hazards analysis demonstrated that the thrombo-inflammatory markers thrombin time, platelet/lymphocyte ratio (PLR), and D-dimer level were independent predictors of mortality. In addition, variables reflecting the severity of CHF (New York Heart Association class > 2), impaired renal function (elevated serum creatinine [SCr]), impaired organ perfusion (elevated BUN), and chronic liver disease were also independent predictors of mortality. Thrombo-inflammatory biomarkers were only weakly associated with SCr and the burden of co-morbidity, suggesting that thrombo-inflammation may in large part be attributable to CHF itself and that, moreover, its presence may confer an increased risk of mortality. Further large-scale prospective studies are needed to determine the existence and the consequences of a thrombo-inflammatory phenotype among patients with CHF.

Renal damage and old age: risk factors for thrombosis in patients with ANCA-associated vasculitis.

Thrombosis in ANCA-associated vasculitis (AAV) was prevalent and has been neglected in Chinese patients. This study tried to describe the clinical characteristics, identify the risk factors, and investigate the causal relationship between AAV and venous thromboembolism (VTE) by two-sample Mendelian randomization (MR) analysis. In this retrospective, observational study, we included all hospitalized AAV patients from Jan 2013 to Apr 2022 in Peking Union Medical College Hospital. We collected their clinical data for multivariate regression analysis to determine the risk factors for thrombosis. The nomogram was constructed by applying these risk factors to predict thrombosis in AAV patients. As for MR analysis, we selected single nucleotide polymorphisms (SNPs) related to AAV from published genome-wide association studies and extracted the outcome data containing deep vein thrombosis (DVT) and pulmonary embolism (PE) from the UK biobank. 1203 primary AAV patients were enrolled, and thrombosis occurred in 11.3%. Multivariate regression suggested that older than 65 years, EGPA, neurological involvement, lung involvement, significantly elevated serum creatinine (> 500µmol/L), and elevated D-dimer were associated with thrombosis in AAV patients. The model demonstrated satisfied discrimination with an AUC of 0.769 (95% CI, 0.726-0.812). MR analysis showed that EGPA could increase the risk of developing DVT and PE (OR = 1.0038, 95%CI = 1.0035-1.0041, P = 0.009). Thrombosis was not rare in Chinese patients with AAV. Renal damage and old age emerged as critical risk factors for thrombosis. EGPA might have a potential causal relationship with DVT and PE.

A retrospective study of clinical profile of para-phenylenediamene poisoning (hair dye poisoning) in cases admitted in medical college

India has a high suicide rate and a large proportion of these suicides occur through poisoning. Poisoning by Hair dye has been increasing and constitutes a large proportion of the poisoning cases. The principle toxic constituent of Hair dye poisoning is Paraphenylenediamine (PPD).Present study was done by analyzing the demographic profile, clinical presentation, biochemical profile, life saving interventions and mortality in cases of PPD poisoning. This study was conducted on 80 cases. Angioedema, pain in oral cavity, dark coloured urine, oro-facial edema were main clinical features. Raised TLC count, elevated liver enzymes (sgpt, sgot), elevated serum creatinine, hypocalcemia, elevated bilirubin, low haemoglobin.Paraphenylene diamine poisoning is developing now days due to easy obtainability and low cheap price. It is more common in poor, illiterate, married females of younger age group living in rural areas. Aggressive treatment and Tracheostomy can save life of Patients.