Duchenne muscular dystrophy (DMD) is an inherited disease characterized by progressive degeneration of the skeletal muscles. Renal dysfunction in patients with DMD has recently become more apparent as life expectancy has increased owing to advances in respiratory devices and heart failure therapies. A 23-year-old man with DMD who required nasal tube feeding was referred to our hospital with a 4-month history of renal dysfunction and anemia. The patient\'s serum creatinine (sCr) level was within the normal range (0.84 mg/dL), but his serum cystatin C level and estimated glomerular filtration rate calculated by cystatin C (5.90 mg/L and 7.5 mL/min/1.73 m2, respectively) indicated severe renal impairment. A urinalysis revealed elevated levels of protein and tubular markers. The patient\'s hemoglobin and erythropoietin levels indicated renal anemia. Hypotension, a collapsed inferior vena cava, and a poor tube feeding episode suggested that the kidney injury was due to renal ischemia, which progressed to tubulointerstitial kidney injury, an intrinsic kidney injury. The angiotensin-converting enzyme inhibitors and beta-blockers were discontinued, and extracellular fluid was infused. Thereafter, the patient\'s renal function recovered. Subsequently, the patient\'s urinary findings and anemia improved. Although advances in cardioprotective agents are expected to improve the prognosis of patients with DMD, it is important to consider that the number of patients with kidney injury due to renal ischemia may increase and that it is difficult to evaluate renal function using sCr level in patients with DMD because of decreased skeletal muscle mass.

Urinary ascites represents a scarcely observed pseudo-acute kidney injury in clinical settings. Protracted or missed diagnosis may hold grave ramifications for patient outcomes.
We reported a case involving an elderly female patient experiencing pseudo-acute kidney injury accompanied by ascites, wherein her renal dysfunction persisted despite medical intervention and hemodialysis. Urinary ascites was identified via a methylene blue test and by contrasting creatinine levels in serum and ascites. This patient\'s kidney function was multiple typified by a marked elevation in serum creatinine/Cystatin C ratio (> 2 L/dL), potentially serving as a clue for the clinical diagnosis of pseudo-acute kidney injury engendered by urinary ascites.
This case suggested the potential diagnostic value of an asynchronous increase in serum creatinine and serum CysC (or an increased ratio of blood creatinine to blood CysC) in patients with pseudo-acute kidney injury.

Elevated creatinine concentrations often indicate acute renal injury and renal biopsies are considered in this situation. However,pseudohypercreatininemia is potential cause of elevated creatinine concentrations, and invasive interventions should be avoided.
A 54-year-old woman underwent surgery for descending aortic dissection.Nine days postoperatively, her creatinine concentration increased from 1 mg/dl to 5.78 mg/dl (normal range, 0.47-0.7 mg/dl). Azotemia and hyperkalemia were absent and physical examination findings were unremarkable. Cystatin C concentration was 1.56 mg/l (normal range, 0.56-0.8 mg/l) and pseudohypercreatininemia was suspected. Testing with different reagents showed a creatinine concentration of 0.84 mg/dl. Immunoglobulin (Ig)G was markedly elevated, and creatinine and IgG fluctuated in parallel, suggesting the cause of the pseudohypercreatininemia. IgG4 was also elevated at 844 mg/dl. Immunosuppressive steroid therapy effectively decreased the IgG concentration and resolved the pseudohypercreatininemia.
In cases of elevated creatinine concentration with the presence of abnormal proteins, pseudohypercreatininemia should be considered. We report a rare case of pseudohypercreatininemia caused by polyclonal IgG.

Sarcoidosis is a multi-organ medical condition that is characterized by the formation of granulomas. We aimed to identify a correlation between each sarcoidosis blood biomarker and cystatin C (Cys-C) in sarcoidosis patients. We report a case of a 60-year-old man with sarcoidosis. The correlation between his Cys-C and each blood biomarker level and that between each blood biomarker and serum creatinine levels were determined using linear regression. Serum Cys-C correlated with each blood biomarker of sarcoidosis, while creatinine did not. These findings suggest that Cys-C is a potential blood biomarker for sarcoidosis.

暂无摘要。

Immunoglobulin A dominant postinfectious glomerulonephritis (IgA PIGN) is a unique medical entity that is rare in the paediatric population. It usually presents with severe renal failure, heavy proteinuria, hypertension, and hypocomplementemia and frequently has an unfavourable prognosis. IgA PIGN generally occurs in association with staphylococcal infections and diabetes mellitus in adult patients. Other pathogens include Escherichia coli and Streptococcus sp. Immunofluorescence studies of kidney biopsy samples show IgA as dominant or codominant antibody.
We encountered a 3-year-old girl with IgA PIGN presenting with acute renal failure, oedema, hypertension, and heavy proteinuria of 7955 mg/g creatinine. Renal biopsy specimens showed diffuse glomerular endocapillary hypercellularity with prominent neutrophil and monocyte infiltration on light microscopy. Strong deposits of IgA and C3 were observed along the glomerular basement membranes and the mesangium by immunofluorescence microscopy, and electron microscopy revealed the presence of subepithelial humps. The patient was managed with steroid (and probatory antibiotic) therapy and is now undergoing follow-up, with a significant improvement 6 months after the initial presentation (glomerular filtration rate (GFR) and cystatin C clearance rate of 165 ml/min/1.73m2 and 106 ml/min/1.73m2, respectively). No signs of bacterial infection were detectable.
This variant of IgA PIGN must be distinguished from other clinical entities, especially IgA nephropathy (mesangial IgA deposits) and postinfectious glomerulonephritis (C3, IgG and occasional IgM capillary loop deposits with or without mesangial distribution), since patients with IgA PIGN may require steroid treatment in addition to antibiotic therapy. Differential diagnosis should also include C3 glomerulopathy. IgA PIGN is a recently identified disease entity that generally manifests in adult patients with both IgA and C3 mesangial and glomerular capillary wall deposits. We present a biopsy-proven case of IgA PIGN that manifested in a patient at an exceptionally young age and that has had a good clinical outcome. To the best of our knowledge, this is the youngest IgA PIGN patient reported thus far.

UNASSIGNED: To identify novel biomarker insulin-like growth factor binding protein-2 (IGFBP-2) associated with preeclampsia (PE) before 20 weeks of gestation and to explore the predictive value of plasma IGFBP-2 in PE.
UNASSIGNED: A prospective nested case-control investigation involving 122 PE patients and 122 normal controls (NC) that were matched 1 : 1 in terms of age and week of pregnancy was carried out in Guangzhou Women and Children\'s Medical Center (Guangzhou, China, 2018030306) from April 2016 to December 2019. At 8 to 20 weeks, blood samples from the mother were taken. To calculate the correlations, univariate conditional logistic regression was employed.
UNASSIGNED: Herein, 12 clinical indices were significantly different between the PE and NC groups (uric acid (UA), cystatin C (Cys C), aspartate aminotransferase (AST), glutamyl transpeptidase (γ-GT), total bilirubin (TB), prothrombin time (PT), red blood cell (RBC), hematocrit (HCT), red cell distribution width (RDW), platelets (PLT), mean platelet volume (MPV), and thrombocytocrit (PCT)). Compared with the NC group (36.79 ± 19.91 pg/mL), the expression level of IGFBP2 in the PE group (19.76 ± 19.40 pg/mL) before 20 weeks of pregnancy was significantly decreased (P < 0.01). Two high-risk factors were found to be significantly associated with PE independently of confounders: anemia 4.35 (2.20-8.45) (P < 0.01) and cesarean section history 8.25 (2.67-26.67) (P < 0.01). As a result of the univariate logistic regression analysis, the following three variables were included in the final logistic regression model.: Y = -18.841 - 0.085 × (IGFBP-2) + 0.630 × (RDW) + 0.165 × (AST) + 0.863 × (MPV). In comparison to IGFBP-2 alone as an independent predictor of PE (AUC = 0.897, 95% CI 0.830-0.964), the model\'s discriminatory power was considerably higher (AUC = 0.953, 95% CI 0.911-0.995).
UNASSIGNED: Plasma IGFBP-2 before 20 weeks of pregnancy combined with high-risk factors and routine blood indexes has a high early predictive value for PE.

Introduction: Chronic kidney disease (CKD) and the number of transgender people is on the rise. Hormone replacement therapy may be associated with the development of adverse effects, including kidney disease. Objective: To report the case of a transgender patient using hormone therapy who developed CKD. Case Report: Male transgender patient, 28 years old, using testosterone cypionate every 15 days, without any comorbidity. Evolved with hypertensive peaks of 160-150/110 mmHg and loss of kidney function (Ur 102 mg/dl, Cr 3.5 mg/dl, estimated Glomerular Filtration Rate (eGFR) of 22 ml/min/1.73m2 considering male gender and 16.6 ml/min/1.73m2 considering female gender). Abdominal ultrasound showed chronic parenchymal nephropathy. Due to the significant reduction in eGFR, the patient was referred for kidney transplantation, but he was not included in the list because he had a creatinine clearance of 23 ml/min/1.73m2 for males and 21.5 ml/min/1.73m2 for females in the most recent tests. Conclusion: Hormone replacement may have contributed to the increase in the patient\'s blood pressure and, consequently, to the development of CKD. There is still no well-established consensus on the best way to estimate the GFR in transgender people, and it seems to be more appropriate to consider the gender to which the person self-identifies or to perform the calculation for both genders, obtaining an estimate of the range in which the patient\'s GFR lies.

Currently there are no biomarkers that are predictive of when patients with type-2 diabetes (T2D) will progress to more serious kidney disease i.e., diabetic nephropathy (DN). Biomarkers that could identify patients at risk of progression would allow earlier, more aggressive treatment intervention and management, reducing patient morbidity and mortality.
Study participants (N=88; control n=26; T2D n=32; DN n=30) were recruited from the renal unit at Antrim Area Hospital, Antrim, UK; Whiteabbey Hospital Diabetic Clinic, Newtownabbey, UK; Ulster University (UU), Belfast, UK; and the University of the Third Age (U3A), Belfast, UK; between 2019 and 2020. Venous blood and urine were collected with a detailed clinical history for each study participant.
In total, 13/25 (52.0%) biomarkers measured in urine and 25/34 (73.5%) biomarkers measured in serum were identified as significantly different between control, T2D and DN participants. DN patients, were older, smoked more, had higher systolic blood pressure and higher serum creatinine levels and lower eGFR function. Serum biomarkers significantly inversely correlated with eGFR.
This pilot-study identified several serum biomarkers that could be used to predict progression of T2D to more serious kidney disease: namely, midkine, sTNFR1 and 2, H-FABP and Cystatin C. Our results warrant confirmation in a longitudinal study using a larger patient cohort.

UNASSIGNED: Targeted cancer therapies have revolutionized the field of oncology by selecting for specific molecular pathways, thus improving overall clinical prognosis. However, many of these targeted treatments have been reported to have adverse kidney effects, including acute kidney injury, interstitial nephritis, and glomerular disease. Furthermore, some of these targeted therapies have also been found to cause an asymptomatic rise in serum creatinine levels through inhibition of active tubular secretion.
UNASSIGNED: A 79-year-old woman was being followed for stage 4 A2 chronic kidney disease secondary to type 2 diabetes and longstanding hypertension. She was diagnosed with invasive mammary carcinoma and was initiated on letrozole, an aromatase inhibitor, and palbociclib, a selective cyclin-dependent kinase inhibitor, was subsequently added. Prior to the initiation of her treatments, her baseline estimated glomerular filtration rate (eGFR) fluctuated between 25 and 28 mL/min/1.73 m2 over the previous year. After initiating palbociclib, her serum creatinine progressively increased, despite having well-controlled blood pressure and diabetes. In addition, there was no history of pre-renal events nor any sonographic evidence of obstruction. Within 7 months, her eGFR based on serum creatinine had decreased down to 12 mL/min/1.73 m2.
UNASSIGNED: Given that there were no clinical or other biochemical changes suggestive of worsening renal function, a serum cystatin C was measured using an immunoturbidimetric assay, which was 1.71 mg/L and correlated with an eGFR of 33 mL/min/1.73 m2 based on the chronic kidney disease epidemiology collaboration (CKD-EPI) cystatin C equation (2012). This value was consistent with her previous baseline. Based on these findings, the significant decrease in eGFR measured by serum creatinine was attributed to the inhibitory effects of palbociclib on tubular creatinine secretion, rather than representing true kidney damage. Thus, a kidney biopsy was not performed in this context.
UNASSIGNED: Seven months later, a repeat serum cystatin C was repeated to assess for any worsening of the patient\'s kidney function and revealed an eGFR of 35 mL/min/1.73 m2 based on the CKD-EPI cystatin C equation (2012), thus revealing stable kidney function and reinforcing the inhibitory effects of palbociclib on tubular creatinine secretion through its direct effects on kidney transporters.
UNASSIGNED: This case report and literature review acknowledges the importance of using alternative methods of assessing kidney function when patients are undergoing targeted cancer therapies known to affect tubular creatinine secretion, which include cyclin-dependent kinase 4/6 inhibitors, poly(adenosine diphosphate-ribose) polymerase inhibitors, tyrosine kinase inhibitors, and mesenchymal-epithelial transition inhibitors. The use of non-creatinine-based markers of glomerular filtration rate (GFR), such as cystatin C and nuclear renal scans, will allow for more accurate estimation of kidney function in the appropriate setting, thus avoiding invasive diagnostic tests and unnecessary adjustments of treatment plans. However, certain targeted cancer therapies have also been proven to cause true kidney injury; therefore, physicians must still maintain a high degree of suspicion and consider invasive investigations and/or cessation or reduction of treatments when alternative measurements of kidney function do not suggest an underestimation of GFR via serum creatinine.
UNASSIGNED: Les thérapies ciblées contre le cancer ont révolutionné le domaine de l’oncologie en sélectionnant des voies moléculaires spécifiques, ce qui améliore le pronostic clinique global. Il a toutefois été rapporté que plusieurs de ces traitements ciblés entraînent des effets indésirables sur les reins, notamment l’insuffisance rénale aiguë, la néphrite interstitielle et la glomérulonéphrite. Qui plus est, certains de ces traitements provoquent aussi une augmentation asymptomatique des taux de créatinine sérique en inhibant la sécrétion tubulaire active.
UNASSIGNED: Une femme de 79 ans était suivie pour une insuffisance rénale chronique de stade 4 A2 secondaire à un diabète de type 2 et à une hypertension de longue date. La patiente été diagnostiquée avec un carcinome mammaire invasif et a reçu du létrozole, un inhibiteur de l’aromatase. Un traitement au palbociclib, un inhibiteur sélectif de la kinase dépendante de la cycline, a été ajouté par la suite. Avant le début du traitement, le DFGe initial de la patiente avait fluctué de 25 à 28 ml/min/1,73 m2 lors de l’année précédente. Après avoir commencé le palbociclib, son taux de créatinine sérique a augmenté progressivement, malgré une pression artérielle et un diabète bien contrôlés. La patiente n’avait aucun antécédent d’événements pré-rénaux ni de preuves échographiques d’obstruction. En sept mois, son DFGe basé sur la créatinine sérique était passé à 12 ml/min/1,73 m2.
UNASSIGNED: En absence de changements cliniques ou biochimiques suggérant une aggravation de la fonction rénale, la cystatine C sérique a été mesurée par dosage immunoturbidimétrique. Son taux (1,71 mg/L) correspondait à un DFGe de 33 ml/min/1,73 m2 obtenu par l’équation CKD-EPI (2012) pour la cystatine C; une valeur comparable à sa référence précédente. À la lumière de ces résultats, la chute significative du DFGe mesurée par la créatinine sérique a été attribuée aux effets inhibiteurs du palbociclib sur la sécrétion tubulaire de créatinine, plutôt qu’à une véritable atteinte rénale. C’est pourquoi une biopsie rénale n’a pas été effectuée.
UNASSIGNED: Après sept mois, la mesure de la cystatine C sérique a été répétée pour évaluer une potentielle aggravation de la fonction rénale. Cette nouvelle mesure a révélé un DFGe de 35 ml/min/1,73 m2 obtenu avec l’équation CKD-EPI (2012) de la cystatine C, ce qui indique une fonction rénale stable et renforce le diagnostic retenu d’un effet inhibiteur du palbociclib sur la sécrétion tubulaire de créatinine dû à ses effets directs sur les transporteurs rénaux.
UNASSIGNED: Ce rapport de cas et la revue de la littérature soulignent l’importance d’utiliser d’autres méthodes d’évaluation de la fonction rénale lorsque les patients suivent des traitements ciblés contre le cancer connus pour affecter la sécrétion tubulaire de créatinine, notamment les inhibiteurs de la kinase dépendante de la cycline (CDK4/6), les inhibiteurs de la polymérase poly-adénosine diphosphate ribose (PARP), les inhibiteurs de la tyrosine kinase (TK) et les inhibiteurs de la transition mésenchymateuse-épithéliale (TEM). L’utilisation de marqueurs du DFG autres que la créatinine, tels que la cystatine C et la scintigraphie rénale nucléaire, permettra une estimation plus précise de la fonction rénale dans le contexte approprié, évitant ainsi des tests diagnostiques invasifs et des ajustements inutiles des plans de traitement. On sait toutefois que certains traitements ciblés contre le cancer sont à l’origine de véritables lésions rénales. Par conséquent, les médecins doivent maintenir un haut degré de suspicion et envisager des examens invasifs et/ou l’arrêt ou la réduction des traitements lorsque d’autres mesures de la fonction rénale ne suggèrent pas une sous-estimation du DFG par la créatinine sérique.