Kidney Essentials

How do I know diabetes is affecting the kidneys?

Season 1 Episode 8

In this episode, Drs. Young, Blaine and Ambruso discuss the diagnosis of diabetic nephropathy and how having diabetic kidney disease impacts an individuals cardiovascular and mortality outcomes.

Sophia Ambruso DO @Sophia_Kidney, Sarah Young MD @kidneycritic, Judy Blaine MD, Parisa Mortaji, MD

Kidney Essentials

Season 1 Podcast episode #8

TITLE: Diabetic Kidney Disease

How do I know if the diabetes has affected the patient's kidneys?

PRESS RECORD

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Welcome to Kidney Essentials!


This is A Podcast for Medical students, residents and all nephrocurious practitioners at the University of Colorado and beyond. We’re here to make nephrology more accessible one podcast at a time. Sarah: “ and sexy!”


Introductions:

Judy:

Sarah: Sarah Young, clinical nephrologist at the university of Colorado and UCH hospitals at the anschutz campus. NO COI twitter handle @kidneycritic

Sophie (list name, COI and twitter handle)


Sophie: Greetings everyone and happy almost spring!! If you haven’t already, please check our out last full episode, Podcast episode #6, which covers all things albuminuria and proteinuria. I think it is a great segway into today’s topic of diabetic kidney disease. Because diabetic kidney disease is such a big topic, we have decided to break it into TWO podcasts. Today we will be discussing epidemiology and pathogenesis. IN our next podcast, we’ll discuss diagnosis and treatment. Exciting…..


On to our case…..


Your primary care colleague consults you for a 45 YO woman with poorly controlled type I diabetes mellitus complicated by diabetic neuropathy, hypertension, creatinine 1.6 and proteinuria.


Judy: How much proteinuria?


Sophie: 800mg/g of albuminuria and 1600mg/g of proteinuria.


Sarah: What did her dipstick show?


Sophie: She has 2++ protein detected on dipstick, and no red blood cells, white blood cells or casts identified on microscopy. 


Judy: Is this progressive?


Yes, the patient urine albumin was previously described as ‘micro albuminuria’ and the patient’s serum creatinine has risen from 0.6mg/dL to 1.1 mg/dL over the last 2 years.


Judy: Does she have retinopathy?


Sophie: yes.


Ok, so let’s just briefly recap from last week, Sarah, what is your diagnosis? Why?


Sarah: 

  • DN  is usually a clinical diagnosis. 
  • 40% patients who have Dm will get diabetic kidney disease (30%TIDM and 40% T2DM).
  • We know she has DM ( we do not know for how long).
  • We know she has other complications of her Dm including neuropathy and retinopathy
  • There is a high correlation between retinopathy and nephropathy
  •  diabetic kidney disease is the leading cause of ckd worldwide...so it is the most likely diagnosis.
  • ...but while this is the clinical dx we are working with there are other diseases that we need to consider (always have a differential) and reassess you assessment regularly


Sophie: Since you’re so confident that this is diabetic nephropathy, would you do anything else to work-up this patient?


Judy:I’d probably perform age appropriate serologic work-up to r/o other causes of proteinuria like HCV, HBV, SPEP, SFLC.


Sophie: Excellent. I’m going to stop there on diagnosis for now and settle on the fact that we’ve made the diagnosis that this patient has diabetic nephropathy. We’ll discuss the criteria for clinical diagnosis later in the podcast.


At this point in time, I’d like to establish a few definitions; What is diabetic nephropathy anyways??


Sarah: Diabetic nephropathy is a patient with diabetes and proteinuria in someone who has pathologic findings consistent with diabetes.



Sophie: so to summarize, diabetic nephropathy refers to albuminuria with specific glomerular changes, correct? Can we have diabetic kidney disease without having diabetic nephropathy and albuminuria?


Sarah/jUdy: Yes


Sophie: What is that called?


Judy: 

Diabetic Kidney Disease, which really is just an all-encompassing term that includes albuminuric diabetic kidney disease and non-albuminuric diabetic kidney disease. The classical clinical course of DKD is characterized by progressive increase in albuminuria followed by decline in GFR. However, there is an emerging non-albuminuric pattern of DKD injury that consists predominantly of tubulointerstitial injury and scarring with non-classical glomerular lesions.

 

Sophie: If it’s all diabetic kidney disease, does it matter if it’s albuminuric or non-albuminuric?


Yes.


Sophie: Why? 


Sarah: 

Non-albuminuric diabetic kidney disease is far more common in type II than type I diabetes

has a slower trajectory of GFR decline.

? Its emergence may be  a reflection of improved management of diabetes and increased use of renin angiotensin aldosterone system (RAAS) blockade, thus reducing microvascular injury, hyperfiltration and hyperglycemic induced injury.

 

Sophie: So, what is the incidence and prevalence of CKD and ESRD in diabetic nephropathy?

 

Judy: Diabetes mellitus (DM) affects 10% of the United States population, 25-30% of whom have diabetic kidney disease. Diabetes is the leading cause of CKD worldwide and DM accounts for 50% of all patients with ESRD. 


Sophie: Wow!! 50% of all patients with ESRD is caused by diabetic kidney disease. Why is it then, that the incidence of ESRD among those with DM is so low?


Sarah: Most patients with diabetic kidney disease die from cardiovascular causes before reaching the need for kidney replacement therapy.I often think of the ESRD patients as the survivors of dm. People associate dialysis with death in part because many patients on hd have really end stage diabetes


Sophie: So, to reiterate, diabetic nephropathy is bad news. Let’s talk more about this, what are the cardiovascular and mortality outcomes in diabetic nephropathy associated CKD?

  

Sarah:

 CKD worsens cardiovascular and non-cardiovascular outcomes in patients with type 1 and 2 DM.

most patients with diabetic nephropathy die of cardiovascular complications prior to reaching the need for kidney replacement therapy. 

DM and CKD together  have an additive effect on cardiovascular risk and mortality. “Rising albuminuria (≥30mg/g) and falling eGFR independently increase the risk for cardiovascular events and death. For every halving of eGFR, the incidence of cardiovascular events is 2-fold higher. For every 10-fold increase in baseline urine albumin, the incidence of cardiovascular events is 2.5-fold higher.”


Sophie: To emphasize one last time, CKD and albuminuria have bad cardiovascular and mortality outcomes in patients with diabetes.


Sophia: our next podcast will cover RAAS, RAAS in DM, I want to briefly touch base on available treatments for diabetic nephropathy.  Judy, what are the goals in managing a patient with diabetic kidney disease.

Tie in glycemic control, 



Key Point

  1. Diabetes is the leading cause of CKD worldwide, accounting for 50% of ESRD.
  2. Diabetic kidney disease dramatically worsening cardiovascular and mortality outcomes
  3. Diabetic nephropathy is a progressive disease, marked by transition from glomerular hyperfiltration to albuminuria to progressive chronic kidney disease and finally, ESKD
  4. Overactive RAAS activity and direct vasoactive activity mediated by TGF lead to disproportional afferent arteriolar vasodilation and efferent arteriolar vasoconstriction, thereby altering glomerular hemodynamics, resulting in hyperfiltration.