Diabetes, Obesity and Heavy Proteinuria

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1 Diabetes, Obesity and Heavy Proteinuria

2 Clinical Case 41 yo Black woman with heavy proteinuria History 2014: noted to have proteinuria on routine lab testing (1.1g/g). 1+ edema. Blood pressure has been difficult to control Proteinuria attributed to obesity / hypertension / type 2 DM Lost to follow-up, presented in 2018 with 11.4g/24hr proteinuria Past Medical History Hypertension (2004) Obesity Type 2 diabetes (Dx 2013) Ovarian cysts / menorrhagia -> hysterectomy

3 Clinical Case 41 yo Black woman with heavy proteinuria Exam VS: Afebrile, P72, BP 178/94 weight 112kg (246lbs) Looked well, obese Chest and heart normal Extremities: 1+ peripheral edema Medications (2018) Aspirin 81mg daily Gemfibrozil 600mg BID Potassium chloride 20mEq BID Metformin 500mg BID Triampterene-HCTZ 37.5 / 25mg alternate days Atorvastatin 40mg qpm Labs Serum creatinine 1.4 mg/dl Potassium 3.4 mmol/l Labetalol 300mg BID Nifedipine ER 60mg daily Valsartan 320mg daily

4 Investigations Blood CBC: Hb 10.7, WBC 9k, platelets 252k Urine UA -ve blood, 3+ protein UPCR: 11.4g/g Sediment: bland, no casts Renal US 11cm kidneys, echogenic

5 Further Investigations Serologies ANA negative Rheumatoid factor <13 Complement levels (normal) C3 108 mg/gl (normal ) C4 12 mg/dl (normal 10-37) Virology: HBV; HCV; HIV negative Paraprotein (negative) sflc mildly elevated (k 3.48; λ 2.37), but ratio1.47 (normal) SPEP with immunofixation: negative

6 DDx?

7 5-12 glomeruli per level section

8 Global glomerulosclerosis involves 63-75% of sampled glomeruli.

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10 FSGS involves 1425% of sampled glomeruli.

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16 Immunofluorescence Microscopye

17 Electron Microscopy What did we see?

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22 FINAL DIAGNOSIS: A-C) Kidney biopsy: 1. Focal and segmental glomerulosclerosis (FSGS) with features of collapsing FSGS. 2. Global glomerulosclerosis, moderate tubular atrophy and interstitial fibrosis, moderate arteriosclerosis and mild arteriolar hyalinosis, likely related to #1.

23 COMMENT: This biopsy demonstrates focal and segmental glomerulosclerosis (FSGS) which involves 1425% of the sampled glomeruli. One of the glomeruli shows features of collapsing FSGS, with partial collapse of the glomerular tuft and hyperplasia of the overlying podocytes/parietal epithelial cells in a corona over the glomerular tuft. Collapsing FSGS can occur in association with infections (HIV, parvovirus B19), medications (pamidronate, calcineurin inhibitor, etc.), vascular ischemic changes, immune complex mediated processes, and as an idiopathic condition. Although the degree of podocyte foot process effacement is not a reliable discriminator between primary and secondary FSGS, the presence of segmental (rather than diffuse) podocyte foot process effacement provides some evidence against a primary podocyte injury process such as primary FSGS. There is a background of significant chronic injury, with global glomerulosclerosis involving 63-75% of sampled glomeruli and a proportional degree of moderate tubular atrophy and interstitial fibrosis. There is no obvious diabetic nephropathy or any evidence of an immune complex process.

24 Differential Diagnosis of Collapsing Glomerulopathy CG associated Diseases Infection* Autoimmune* Malignancy Ischemia Genetic Drug exposure HIV, cytomegalovirus, parvovirus B19, pulmonary TB, leishmaniosis, malaria Adult Still's disease, systemic lupus erythematosis, mixed connective tissue disorder, cerebral arteritis Hemophagocytic syndrome*, multiple myeloma, acute monoblastic leukemia Thrombotic microangiopathy, peri-infarct, cholesterol embolism ApoL1 high risk alleles, mitochondrial cytopathies, action myoclonus-renal failure syndrome, familial, sickle cell disease Interferons* (alpha, beta, or gamma); anabolic steroids, bisphosphonates, calcineurin inhibitors IgA nephropathy, diabetic glomerulopathy, Lupus nephritis Superimposed on other *inflammatory diseases

25 Clinical Presentation: Idiopathic CG Detweiler RD et al (1994) Valeri A et al (1996) Cossey LN et al (2017)* Series n=16, Chapel Hill, NC n=43, Columbia, NY n = 88, Little Rock, AR Age (at biopsy) 42 yrs 32 yrs 43 yrs Black 81% 61% (17% W, 22% Hispanic) 84% Nephrotic syndrome 56% 91% 86% Hypertension 56% 68% 92% Proteinuria 7.7g/d 10.2g/d 11g/d Serum creatinine 3.5 mg/dl 4.2 mg/dl 4.2 mg/dl ESRD 43% by 12m 50% by 32m - * Includes 15 patient with HIV

26 Kidney International (2008) 74,

27

28 Take Home Message Discrimination between a primary vs. secondary FSGS is not always straightforward based on the extent of foot process effacement. Pitfalls: Extensive foot process effacement can be seen in ischemic glomeruli and in glomeruli with FSGS Extensive foot process effacement in intact glomeruli + supportive clinical findings (nephrotic range proteinuria, especially if not gradually rising and no other comorbidities): likely primary FSGS Segmental foot process effacement if associated with hilar FSGS, gradual rise in proteinururia or other comorbidities (HTN, diabetes, obesity, etc.): most likely secondary FSGS

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