In the NEWS: Obesity Related CKD

Obesity-related Chronic Kidney Disease (Ob-CKD) encompasses a wide range of manifestations in persons with chronic kidney disease (CKD), from cases without known structural damage (hyperfiltration or albuminuria) to more advanced stages with obesity-related glomerulopathy (glomerular hypertrophy, podocytopathy, mesangial matrix expansion, focal and segmental glomerulosclerosis, tubulointerstitial fibrosis, tubular atrophy, and vascular lesions). Ob-CKD can also coexist with other kidney diseases, affect persons on dialysis, and in kidney transplant recipients.

In response to this complexity, Spanish Society of Nephrology (S.E.N.), Latin American Society of Nephrology and Hypertension (SLANH), and Spanish Society for the Study of Obesity (SEEDO) developed a consensus report proposing a classification system based on renal alterations and CKD stage (non-dialysis, dialysis, or transplant), aiming to standardize terminology and guide clinical management.  One of our principal aims is to diagnose individuals with obesity and CKD, classify, and subsequently individualize their treatment. What remains undiagnosed will remain untreated.

The effective treatment of Ob-CKD requires a multidisciplinary approach involving nutritional therapy, physical activity, pharmacological treatment, and bariatric surgery when indicated. The consensus also emphasizes the role of incretin-based therapies, which have been shown to promote weight loss and improve cardiorenal outcomes, including reductions in cardiovascular events and mortality in persons with Ob-CKD.

This was published in Kidney International 

See a sample below of cases related to Ob-CKD

Guest Post by

Dr. Maria J Soler

In the News: A new virus- Pegivirus induced CNS disease in organ transplants

A letter in NEJM describes a potential new neurological disease, pegivirus-associated encephalomyelitis (PAEM), linked to the common virus Pegivirus hominis (HPgV-1).  Four immunosuppressed patients presented with progressive optic neuropathy and myelopathy, including spastic paraparesis or tetraparesis and sensory disturbances. 

Two patients died within two years of symptom onset, while the others remained severely disabled.  MRI scans revealed a distinctive pattern of bilateral, symmetrical lesions in the anterior visual pathway and spinal cord's corticospinal tracts and posterior columns.  

HPgV-1 was detected in the patients' cerebrospinal fluid, serum, and brain tissue, but not in controls, suggesting a causative role.  Viral loads were highest in the optic nerve and spinal cord, and genomic sequencing revealed compartmentalization within the CNS, further supporting this link.  

The authors propose that PAEM, characterized by these specific clinical, radiological, and virological findings, may be underdiagnosed and that characteristic MRI findings should prompt HPgV-1 testing.

The appendix includes in-depth methods, results, discussion, and individual patient case reports.  It elaborates on the clinical presentation, MRI and CSF findings, HPgV-1 RNA detection and quantification, and full-genome sequencing analysis supporting viral compartmentalization within the CNS. Two of the 4 patients were renal transplant recipients. 

One of them was a  57-year-old kidney transplant recipient due to pANCA-associated vasculitis, presented with progressive hypoesthesia and weakness in his legs, followed by vision loss, nausea, vomiting, and cognitive difficulties. He was on CNI, MMF and steroids and had received cyclophosphamide in the past.  He developed bladder and bowel dysfunction and lost the ability to walk. MRI showed abnormalities in the optic nerves, chiasm, pyramids, and spinal cord. HPgV-1 RNA was detected in both serum and CSF.  Despite immunosuppression reduction and treatment with ribavirin, his condition didn't improve, and he died 17 months after symptom onset.  Autopsy revealed myelin loss, glial cell abnormalities, and T-cell and macrophage infiltration in affected brain regions. Viral loads were highest in the optic nerve and cervical spinal cord.

Another patient was a 62-year-old kidney transplant recipient due to polycystic kidney disease, experienced progressive paresthesia and leg weakness, leading to spastic tetraparesis.  She was on mTORi, Steroids and belatacept.  She later experienced vision loss. Spinal MRI revealed lesions in the cervical and upper thoracic spinal cord.  HPgV-1 RNA was detected in both serum and CSF.  Belatacept was discontinued, and she was maintained on methylprednisolone and later azathioprine.  Her condition was complicated by aspiration pneumonia, infections, and renal graft failure requiring ICU care.  While her neurological symptoms partially improved, allowing for ventilator weaning and improved arm strength, she remained paralyzed in her legs and required dialysis.  Follow-up revealed no HPgV-1 RNA in serum but persistent presence in CSF.

This new virus will require us to be more vigilant in the transplant world and perhaps even in the world of immunosuppression. 

Detective Nephron: Next venture

 

Check out the next Detective Nephron as we tackle a fun case

Concept Map: Risk factors for Calcific uremic arteriolopathy ( Calciphylaxis)

 

Diabetic Nephropathy 2025 Review of new agents

 

Inspired by a recent talk I listened to by Dr. Marteen Taal

Concept Map: Cryoglobulinemia

 Here is a summary via pics on Cryoglobulinemia. Check out a review on this in NEJM.

Top 10 things Nephrologists Wish every Primary Care and Hospitalists Knew

1. A “Normal” Serum Creatinine Level May Not Be Normal

2. Patients With Decreased GFR or Proteinuria Should Be Evaluated to Determine the Cause; Positive Urine Dipstick Test Results for Protein Should Be Followed Up With a Spot Urine Protein or Albumin to Urine Creatinine Ratio.

3. A low Potassium level -- please check a magnesium level as well as hypomagnesemia leads to hypokalemia

4. Know the Medications That Spuriously Elevate the Serum Creatinine Level. A cystatin C-based GFR may help in this matter.

5. Do Not Automatically Discontinue an ACEI /ARB or SLGT2i Solely Because of a Small Increase in the Serum Creatinine or Potassium Level.

6. Not all elevations in Potassium are real- in the right context make sure you rule out hemolysis, hyperglycemia and pseudohyperkalemia before freaking out!

7. Although Most Patients With Hypertension are essential, a simple urinalysis may help diagnose a renal cause. HTN may be a symptom of underlying renal disease in many cases.

8. PPIs cause heart burn for the Nephrologists. Stop if no strong indication as they cause AKI and CKD.

9. Do not change dialysis schedule for ESKD patients for a contrast study( they are end-stage already).

10.If the Na is low, make sure the patient is not getting antibiotics or other meds in D5W and if the Na is high, make sure the patient is not getting meds in normal saline.