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Nephrotic Syndrome

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Nephrotic Syndrome GRANT GALLIMORE, MD, MAJ, USAF, MC NEPHROLOGY CHIEF, KEESLER MEDICAL CENTER Overview o History and terminology o Major causes of nephrotic syndrome and prevalence o Patient presentation, history and exam o Laboratory and imaging based on potential etiology o Selected pathology and microscopy o Complications and management History and Terminology o Nephrotic was coined in 1905 by Friedrich von Müller, a distinguished German Pathologist o The term nephrotic syndrome is attributed to Louis Leiter of the University of Chicago, using the term in a widely read review in 1930 o Percutaneous renal biopsy was introduced in 1951, resulting in description of many distinct disease entities Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. History and Terminology o Berman and Schreiner 1958 biopsy series threshold of 3.5g/24h was determined o All patients had hypoalbuminemia and oval fat bodies in urine o Edema was absent in 27% and hyperlipidemia absent in 25% Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. History and Terminology o Definition should be based on 24h urine excretion of protein rather than albumin, although 60-90% of proteinuria should be albumin o Many conditions can give rise to nephrotic range proteinuria but not to nephrotic syndrome o With preserved albumin, responsible lesions are likely to result from secondary processes like hyperfiltration, obesity, nephron loss o For example, the majority of African Americans with FSGS have nephrotic-range proteinuria but not nephrotic syndrome Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Sara Conti, Norberto Perico, et al. Early and late scanning electron microscopy findings in diabetic kidney disease. Scientific Reports 8, Article number: 4909 (2018) https://doi.org/10.1038/s41598-018-23244-2 Sara Conti, Norberto Perico, et al. Early and late scanning electron microscopy findings in diabetic kidney disease. Scientific Reports 8, Article number: 4909 (2018) https://doi.org/10.1038/s41598-018-23244-2 Figure 3 American Journal of Kidney Diseases 2015 66, 376-377DOI: (10.1053/j.ajkd.2015.04.006) Copyright © 2015 National Kidney Foundation, Inc. Terms and Conditions Patient History o Wide spectrum varying from asymptomatic to life-threatening disease o The following historical elements may be relevant: oSystemic disease o SLE, RA, Crohn’s, DM, HTN, obesity, nephron loss, frequent UTI o Family history o FSGS, complement disorders o Medications o NSAIDs, interferon, bisphosphonates o History of malignancy o Breast, lung, gastrointestinal, lymphoma o History of infection o HIV, Hepatitis B or C, syphilis, malaria Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Exam o Edema is often periorbital in the morning (no orthopnea) o This is in contrast to heart failure (pulmonary congestion producing orthopnea) and cirrhosis (diaphragmatic pressure from ascites) o Massive weight gain is common, with fluid overload including ascites, pleural effusions, abdominal and genital edema o Muehrcke lines and xanthelasma may be seen o Palpable purpura in vasculitis, SLE, cyroglobulinemia Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Parvovirus Metabolic, Autoimmune, Infectious, Neoplastic, Drugs Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Laboratory o Consider serology for Hepatitis B (MN) and C (MPGN), HIV (FSGS) o Low C3/C4 may be seen in SLE, MPGN, infection-associated, dense deposit disease, HUS o ANA to screen SLE as a cause of membranous o RF may be positive due to RA (MN, amyloid) or cryoglobulinemia o SPEP and serum free light chains may reveal paraprotein-associated disease whether myeloma, amyloidosis, or others Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Imaging o Ultrasound scanning to ensure 2 kidneys, rule out obstruction or anatomic abnormalities o Large kidneys (>14cm) may suggest diabetic nephropathy, amyloid disease, HIV, acute severe GN, or AIN o Small kidneys (<9cm) and/or cortical thinning should limit enthusiasm for biopsy or aggressive immunosuppression Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Figure 2 American Journal of Kidney Diseases 2015 66, 376-377DOI: (10.1053/j.ajkd.2015.04.006) Copyright © 2015 National Kidney Foundation, Inc. Terms and Conditions Couser WG. Primary Membranous Nephropathy. CJASN June 2017, 12 (6) 983-997; DOI: https://doi.org/10.2215/CJN.1176111 Membranous Nephropathy Beck LH et al. N Engl J Med 2009; 361: 11-21. FSGS light microscopy patterns Focal Segmental Glomerulsclerosis [Internet]. [cited 2019 Jul 5]. Available from https://unckidneycenter.org/kidneyhealthlibrary/glomerular-disease/focal-segmental-glomerulosclerosis-fsgs/ Complications and Management Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Edema formation o Overfill is actually much more common than underfill o This seems to be related to activation of the epithelial sodium channel (ENaC) by proteolytic enzymes in tubular lumen o Leads to increased blood volume, RAAS suppression, tendency to hypertension o Increased blood volume with low oncotic pressure leads to transudation of fluid into interstitium Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Edema formation o The argument for overfill theory o Individuals lacking serum albumin often do not have sodium retention o During recovery, natriuresis occurs prior to improvement in hypoalbuminemia o IV albumin does not consistently improve natriuresis o Studies with radioactive albumin have demonstrated low plasma and blood volumes in as few as 2% of cases o Adrenalectomized rats with nephrotic syndrome have sodium retention o Proteases such as plasminogen have been shown to activate ENAC Ray, E. C., Rondon-Berrios, H., Boyd, C. R., & Kleyman, T. R. (2015). Sodium Retention and Volume Expansion in Nephrotic Syndrome: Implications for Hypertension. Advances in Chronic Kidney Disease, 22(3), 179-184. doi:10.1053/j.ackd.2014.11.006 Treatment of edema o Diuretic efficacy is likely to be impaired o Transport from peritubular capillaries requires protein binding o Increased protein binding in tubular lumen limits access to transporters o Gastrointestinal absorption may be limited o Ways to overcome diuretic resistance o Use of IV therapy o Use of thiazide in addition to loop diuretic with close monitoring o Addition of amiloride (ENaC highly relevant to pathophysiology) o Consideration of IV albumin Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Addition of thiazide Addition of amiloride Use of IV therapy Use of albumin Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Response to hypoalbuminemia o Increased protein synthesis is not discriminating, as the synthesis of many proteins other than albumin is upregulated o This includes large molecular weight proteins that are not filtered and may actually increase in concentration o This has implications for both hyperlipidemia and hypercoagulability Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen,
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  • Chapter 10: Radiation Nephropathy

    Chapter 10: Radiation Nephropathy

    Chapter 10: Radiation Nephropathy † Amaka Edeani, MBBS,* and Eric P. Cohen, MD *Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland; and †Nephrology Division, Department of Medicine, University of Maryland School of Medicine, and Baltimore Veterans Affairs Medical Center, Baltimore, Maryland INTRODUCTION Classical radiation nephropathy occurred after external beam radiation for treatment of solid The occurrence of renal dysfunction as a consequence cancers such as seminomas (6); the incidence has of ionizing radiation has been known for more than declined with the advent of more effective chemo- 100 years (1,2). Initial reports termed this condition therapy. In recent years, radiation nephropathy has “radiation nephritis,” but that is a misnomer, because occurred due to TBI used as part of chemo-irradiation it is not an inflammatory condition. Renal radiation conditioning just before hematopoietic stem cell injury may be avoided by the exclusion of an ade- transplantation (HSCT) and also from targeted ra- quate volume of kidney exposure during radiation dionuclide therapy used for instance in the treatment therapy, but the kidneys’ central location can make of neuroendocrine malignancies. TBI may be myelo- this difficult to impossible when tumors of the abdo- ablative or nonmyeloablative, with myeloablative men or retroperitoneum are treated, or during total regimens using radiation doses of 10–12 Gy to de- body irradiation (TBI) (3). stroy or suppress the recipient’s bone marrow. These doses are given in a single fraction or in nine fractions over 3 days (4). In addition, TBI for bone marrow BACKGROUND/CLINICAL SIGNIFICANCE transplantation (BMT) is preceded or accompanied by cytotoxic chemotherapy, which potentiates the Radiation nephropathy is renal injury and loss of effects of ionizing radiation (7).