Membranous nephropathy

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Membranous nephropathy

Pathology

Renal and ureteral disorders

Renal agenesis

Horseshoe kidney

Potter sequence

Hyperphosphatemia

Hypophosphatemia

Hypernatremia

Hyponatremia

Hypermagnesemia

Hypomagnesemia

Hyperkalemia

Hypokalemia

Hypercalcemia

Hypocalcemia

Renal tubular acidosis

Minimal change disease

Diabetic nephropathy

Focal segmental glomerulosclerosis (NORD)

Amyloidosis

Membranous nephropathy

Lupus nephritis

Membranoproliferative glomerulonephritis

Poststreptococcal glomerulonephritis

Goodpasture syndrome

Rapidly progressive glomerulonephritis

IgA nephropathy (NORD)

Lupus nephritis

Alport syndrome

Kidney stones

Hydronephrosis

Acute pyelonephritis

Chronic pyelonephritis

Prerenal azotemia

Renal azotemia

Acute tubular necrosis

Postrenal azotemia

Renal papillary necrosis

Renal cortical necrosis

Chronic kidney disease

Polycystic kidney disease

Multicystic dysplastic kidney

Medullary cystic kidney disease

Medullary sponge kidney

Renal artery stenosis

Renal cell carcinoma

Angiomyolipoma

Nephroblastoma (Wilms tumor)

WAGR syndrome

Beckwith-Wiedemann syndrome

Bladder and urethral disorders

Posterior urethral valves

Hypospadias and epispadias

Vesicoureteral reflux

Bladder exstrophy

Urinary incontinence

Neurogenic bladder

Lower urinary tract infection

Transitional cell carcinoma

Non-urothelial bladder cancers

Renal system pathology review

Congenital renal disorders: Pathology review

Renal tubular defects: Pathology review

Renal tubular acidosis: Pathology review

Acid-base disturbances: Pathology review

Electrolyte disturbances: Pathology review

Renal failure: Pathology review

Nephrotic syndromes: Pathology review

Nephritic syndromes: Pathology review

Urinary incontinence: Pathology review

Urinary tract infections: Pathology review

Kidney stones: Pathology review

Renal and urinary tract masses: Pathology review

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Membranous nephropathy

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Membranous nephropathy

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A 52-year-old female comes to the primary care physician due to worsening weight gain. She has gained approximately 20 lbs over the past six weeks. In addition, the patient has been experiencing lower extremity edema and has noticed her urine appears more cloudy than usual. Past medical history is notable for hypertension and hyperlipidemia. Temperature is 37.3°C (99.1°F), pulse is 76/min, respirations are 18/min, blood pressure is 137/84 mmHg, and O2 saturation is 97% on room air. Physical exam is notable for bilateral pitting edema of the lower extremities. A urinalysis is notable for 4+ protein and oval fat bodies but no hematuria. A renal biopsy is performed, and the following is visualized on light microscopy:  


Reproduced from: Wikipedia  
Which of the following is most suggestive of this patient’s underlying diagnosis?  

External References

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Membranous nephropathy p. 618, 619, 723

membranous nephropathy, primary

autoantibody p. 113

Transcript

Content Reviewers

Rishi Desai, MD, MPH

Contributors

Tanner Marshall, MS

Membranous glomerulonephritis, also known as membranous nephropathy, is where the glomerular basement membrane, or GBM, which lines the glomeruli in the kidney, becomes inflamed and damaged, which results in increased permeability and proteins being able to filter through into the urine, causing nephrotic syndrome.

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules, like sodium and water, move from the blood into the kidney nephron, where it eventually makes its way into the urine. But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria, typically greater than 3.5 grams per day.

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood.

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema.

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids, or fat, you get increased levels of lipid in the blood, called hyperlipidemia.

Just like the proteins, these lipids can also get into the urine, causing hyperlipiduria.

And those are the hallmarks of nephrotic syndromeproteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Alright, so with membranous glomerulonephritis, the basement membrane becomes damaged which causes nephrotic syndrome. How does this happen, though? Well, ultimately this damage is caused by immune complexes—complexes composed of an antigen with an antibody bound to it.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Membranous nephropathy in children: clinical presentation and therapeutic approach" Pediatric Nephrology (2009)
  6. "Thrombospondin Type-1 Domain-Containing 7A in Idiopathic Membranous Nephropathy" New England Journal of Medicine (2014)
  7. "Immunosuppressive treatment for idiopathic membranous nephropathy in adults with nephrotic syndrome" Cochrane Database of Systematic Reviews (2014)
  8. "Membranous Glomerulopathy: Emphasis on Secondary Forms and Disease Variants" Advances in Anatomic Pathology (2001)
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