Lupus nephritis

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Lupus nephritis

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Development of the renal system
Ureter, bladder and urethra histology
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Renal system anatomy and physiology
Body fluid compartments
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Horseshoe kidney
Renal agenesis
Potter sequence
Posterior urethral valves
Multicystic dysplastic kidney
Polycystic kidney disease
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Alport syndrome
Urinary incontinence
Urinary incontinence: Pathology review
Neurogenic bladder
Bladder exstrophy
Antidiuretic hormone
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Diabetes insipidus and SIADH: Pathology review
Diabetes insipidus
Nephrotic syndromes: Pathology review
Nephritic and nephrotic syndromes: Clinical
Nephritic syndromes: Pathology review
Minimal change disease
Hydronephrosis
Glomerular filtration
Measuring renal plasma flow and renal blood flow
Renal clearance
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Sodium homeostasis
Kidney countercurrent multiplication
Urea recycling
Tubular reabsorption and secretion
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Tubular reabsorption of glucose
Distal convoluted tubule
Loop of Henle
Proximal convoluted tubule
Renin-angiotensin-aldosterone system
Free water clearance
Amyloidosis
IgA nephropathy (NORD)
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
Lupus nephritis
Potassium homeostasis
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Hypernatremia
Phosphate, calcium and magnesium homeostasis
The role of the kidney in acid-base balance
Acid-base disturbances: Pathology review
Physiologic pH and buffers
Renal tubular acidosis
Renal tubular acidosis: Pathology review
Metabolic acidosis
Metabolic and respiratory acidosis: Clinical
Respiratory acidosis
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Plasma anion gap
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Acid-base map and compensatory mechanisms
Ornithine transcarbamylase deficiency
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Nitrogen and urea cycle
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Erythropoietin
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Renal tubular defects: Pathology review
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Urinary tract infections: Pathology review
Lower urinary tract infection
Proteus mirabilis
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Renal artery stenosis
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Renal failure: Pathology review
Renal and urinary tract masses: Pathology review
Transplant rejection
Graft-versus-host disease
Non-corticosteroid immunosuppressants and immunotherapies
Hypertension
BK virus (Hemorrhagic cystitis)

Transcript

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The termlupus’ refers to systemic lupus erythematosus, ‘nephritis’ refers to the ‘nephron,’ the Greek word for kidney, and ‘itis’ means inflammation, so lupus nephritis refers to inflammation of the kidney that results from having systemic lupus erythematosus.

Lupus is an autoimmune disease in which the immune system attacks various parts of the body, including the skin, joints, lungs, heart, central nervous system, and, of course, the kidneys.

In fact, about half of all individuals with lupus develop some form of lupus nephritis.

In lupus, what happens is that some cells have their DNA so badly damaged, that the cell undergoes programmed cell death, or apoptosis, and it dies. This produces all these little apoptotic bodies, and exposes the insides of the cell, including parts of the nucleus, like DNA, histones, and other proteins, to the rest of the body.

Now in lupus the immune system is more likely to think that cellular parts are foreign, or antigens, and since they’re from the nucleus, their referred to as nuclear antigens, and immune cells try to attack them.

Not only that though, individuals with lupus have less effective clearance, essentially they aren’t as good at getting rid of the apoptotic bodies and so they end up having more nuclear antigens floating around.

So as a result of all of this, B cells start producing antibodies against these pieces of nucleus, which are called antinuclear antibodies.

These antinuclear antibodies bind to nuclear antigens, forming antigen-antibody complexes, which drift away in the blood and deposit in various places including the kidneys.

These immune complexes can then initiate an inflammatory reaction, which is known as a type III hypersensitivity reaction.

Lupus nephritis is classified into various types depending on the exact site of these immune complexes and subsequent inflammatory reaction. The most common site of deposition is just underneath the capillary wall, also known as the endothelium, but deposits can also be within the Bowman’s space of the nephron, the basement membrane, or near the mesangial cells.

The extent of inflammation within the kidney can be focal, involving nephrons in just one area, or diffuse, involving almost all of the nephrons in both kidneys.

In the majority of cases lupus nephritis presents as a nephrotic syndrome, which means that the damage to the nephron allows plasma proteins to get into the urine, which causes proteinuria—typically greater than 3.5 grams per day.