Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease (ESKD) in the United States. Risk factor modification, such as tight control of blood glucose, management of hypertension and hyperlipidemia, and the use of renin–angiotensin–aldosterone system (RAAS) blockade have been proven to help delay the progression of DKD. In recent years, new therapeutics including sodium-glucose transport protein 2 (SGLT2) inhibitors, endothelin antagonists, glucagon like peptide-1 (GLP-1) agonists, and mineralocorticoid receptor antagonists (MRA), have provided additional treatment options for patients with DKD. This review discusses the various treatment options available to treat patients with diabetic kidney disease.

Diabetic kidney disease (DKD) is a complication of diabetes that can lead to kidney failure. Over the years, several drugs have been developed to combat this disease. In the early 90s, angiotensin blockade (ACEi and ARBs) was introduced, which revolutionized the treatment of DKD. In recent years, newer drugs such as sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, endothelin antagonists, and mineralocorticoid receptor antagonists (MRA) have shown great promise in reducing albuminuria and protecting the kidneys. These drugs are being used in combination with lifestyle modifications, patient education, and risk factor modification to effectively manage DKD. In this review, we will explore the latest pharmacological options, their efficacy, and their potential to revolutionize the management of this debilitating disease.

Key Points: Oxalate nephropathy is an underrecognized cause of CKD and ESKD We present one of the largest native oxalate nephropathy cohorts to date from a tertiary care institution in the United States Oxalate nephropathy has multiple etiologies and given its clinical course and poor prognosis, attention must be paid to screening for risk factors to guide prompt diagnosis and management Background: Oxalate nephropathy (ON) is characterized by deposition of calcium oxalate crystals in the kidney and is commonly under-recognized. Causes of ON include primary hyperoxaluria, enteric hyperoxaluria, and ingestion of excess oxalate or its precursors. Methods: We report the clinical and pathological characteristics of one of the largest series of native kidney ON to date, from January 2015 to March 2023 at the Cleveland Clinic. Results: We identified 60 native biopsies with oxalate deposits and excluded patients with clinically insignificant biopsies ( n =12) or lack of data ( n =17). Thirty-one patients with native ON were described. The mean age at diagnosis was 66.2 years (±12.1), and 58.1% were female. 87.1% had hypertension, 58.1% had diabetes, 42% had nephrolithiasis, and 77.4% had underlying CKD, with a mean baseline creatinine of 1.8 mg/dl ±1.3. The mean creatinine at biopsy was 5.2 mg/dl ±1.7. Kidney biopsies showed abundant calcium oxalate crystal deposits, and 27 of 31 biopsies had additional diagnoses, the most common of which were acute tubular injury n =17 (54.8%) and diabetic glomerulosclerosis n =7 (22.6%). Severe and moderate interstitial fibrosis was present in 38.7% ( n =12) and 51.6% ( n =16) of biopsies, respectively. Ten had a single etiology of ON, ten had a multifactorial etiology (both enteric hyperoxaluria and high precursor intake), and 11 had an unclear etiology. Notably, only seven patients had a history of gastric bypass. The mean duration of follow-up was 26.8 months, and 26 patients had follow-up data >1 year. Of these, 21 required dialysis, and five were dialysis-free at presentation. Five of the 26 were deceased at 1 year, with 12 patients (38.7%) deceased at last follow-up. Seventeen patients received targeted management, while nine patients did not receive targeted treatment, and all nine required hemodialysis. More patients (31.6%) had vitamin C intake after the coronavirus disease 2019 pandemic (2020–2023) versus 16.7% before 2020. Conclusions: ON presents as AKI or acute on CKD. The prognosis is poor with most patients requiring dialysis at presentation with high morbidity and mortality. Clinicians need to be aware of the risk factors associated with ON to aid prompt diagnosis and management. Podcast: This article contains a podcast at https://dts.podtrac.com/redirect.mp3/www.asn-online.org/media/podcast/K360/2024_01_26_KID0000000000000340.mp3

Background: A non-tunneled dialysis catheter (nTDC) is often the vascular access of choice to initiate dialysis in an intensive care unit (ICU). In the absence of contraindications, if a patient remains dialysis dependent beyond 2-weeks, the options are either to replace the nTDC with another nTDC or convert to a tunneled dialysis catheter (TDC). As a standard of care, TDCs are placed under fluoroscopic guidance. Objectives: To determine if TDCs and other tunneled central venous catheters (tCVC) can be placed safely using anatomical landmark techniques without the use of fluoroscopy. Research design: Subjects that met a predetermined selection criteria underwent placement of tunneled catheters with the use of the anatomical landmark technique. We looked at various outcomes to determine the safety and effectiveness of this technique. Subjects: One hundred eleven TDCs and other tCVCs were placed using the anatomical landmark technique in the intensive care unit. Results: All but one (110/111) of the catheters placed had recommended tip placement confirmed by at least one blinded physician. Major complications encountered were bleeding (two cases), pneumothorax (one case), and line associated blood stream infection (one case). We did find a higher-than-expected rate of “unnecessary procedures” with 18/111 lines placed in patients who did not survive beyond 7 days after placement of the catheter. Conclusions: Using the anatomical landmark technique for bedside tunneled catheter placement can be an effective approach in the right population.

IgA nephropathy is a common cause of glomerular disease that may result in kidney failure. Until recently, angiotensin blockade using angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) were the main treatment options for patients with IgA nephropathy. Newer drugs such as sodium-glucose co-transporter 2 (SGLT2) inhibitors, endothelin angiotensin receptor antagonists (DEARA), endothelin receptor antagonists (ERA), complement inhibitors, targeted release formulation glucocorticoids, and a proliferation-inducing ligand (APRIL) and B cell activation factor (BAFF) inhibitors have shown promise in reducing proteinuria and delaying the progression of IgA nephropathy. In this review, we will explore the latest pharmacological options, their efficacy, and when they should be considered in adult patients with IgA nephropathy.