Diffuse proliferative nephritis

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Diffuse proliferative nephritis
Other namesGlomerulonephritis
Specialty Nephrology

Diffuse proliferative glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. [1] In absence of SLE, DPGN pathology looks more like Membranoproliferative glomerulonephritis [ citation needed ]

Contents

In DPGN Most of the glomeruli show endothelial and mesangial proliferation, affecting the entire glomerulus, leading to diffuse hypercellularity of the glomeruli, producing in some cases epithelial crescents that fill Bowman's space. When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid "wire loops" on routine light microscopy. Immune complexes can be visualized by staining with fluorescent antibodies directed against immunoglobulins or complement, resulting in a granular fluorescent staining pattern. Electron microscopy reveals electron-dense subendothelial immune complexes (between endothelium and basement membrane). In due course, glomerular injury in DPGN gives rise to scarring (glomerulosclerosis). Most of SLE patients with DPGN have hematuria with moderate to severe proteinuria, hypertension, and renal insufficiency. [2]

Signs and Symptoms

Symptoms can be caused directly from DPGN or from a different disease that is causing DPGN. Many of the symptoms, like edema and hypertension, occur due to the decrease in glomerular filtration rate. [3]

Patients can experience general systemic symptoms including fatigue, vomiting, nausea. These would all indicate uremia. [4]

Other patients can experience:

DPGN caused by other diseases

If a patient has DPGN due to IgA nephropathy (Berger Disease) then they can experience flank pain, gross hematuria, and upper respiratory infections.[ citation needed ]

If a patient has DPGN with underlying anti-GBM then they can experience alveolar hemorrhage and respiratory issues.[ citation needed ]

If a patient has DPGN with an underlying autoimmune disease then the patient can experience photosensitivity, rash, joint pains, serositis, and oral ulcers. [4]

Cause

The cause of diffuse proliferative glomerulonephritis (DPGN) depends on the severity of the disease. DPGN is a secondary disease, in that a disease that a patient already has causes DPGN to occur. The most common associated disease of DPGN is severe systemic lupus erythematosus(SLE). [4] Specifically, Lupus nephritis class IV. [5] The other commonly associated disease is Immunoglobulin A (IgA) nephropathy. Post-infectious glomerulonephritis can also be caused by bacterial or viral infections. Streptococcal throat or skin infection is most commonly seen as the origin if glomerulonephritis is going to be caused by an infection. [6] Other causes of DPGN are endocarditis, Hepatitis B, and Hepatis C. [ citation needed ]

Diffuse Proliferative Lupus Nephritis class IV Diffuse proliferative lupus nephritis.jpg
Diffuse Proliferative Lupus Nephritis class IV
Micrograph image of increased mesangial matrix and mesangial hypercellularity due to diffuse proliferative lupus nephritis Diffuse proliferative lupus nephritis - high mag.jpg
Micrograph image of increased mesangial matrix and mesangial hypercellularity due to diffuse proliferative lupus nephritis

Pathophysiology

The etiology plays a role in the specific mechanism of DPGN. Usually the deposition of immune-complexes (antigen-antibody complex) that activates the complement system are involved. [4] The antibodies that form immune complexes deposits or they bind directly to the nonglomerular antibodies present. Immune-complexes are combinations of DNA, anti-dsDNA ubiquitin, and other proteins in DPGN that are associated with lupus nephritis. C1q, the first component of the complement system, encounters conformational change that leads to C3 convertase breaking C3 into C3a and C3b. C3a, C5a, IL-8 are all chemotactic factors of the activated complement system. Part of their role is to recruit polymorphonuclear cells and leukocytes. Interleukins like IL-6, tumor necrosis factor-alpha, and interferon-gamma, that cause cell injury, are released. Mesangial proliferation is caused by activated platelets. [7] Another mechanism involves antibodies formed against alpha-3 chain of collagen IV. Their deposition occurs in the sub-epithelial spaces. This causes proteinuria by damaging the basement membrane and creating a loss of negative charge. These are anionic deposits that fail to cross the membrane. [4]

Cationic deposits that cross the membrane are then deposited into sub-epithelial spaces. Then the disease advances and crescents are formed. Crescents are a combination of epithelial cells, activated macrophages, and fibrin. They lead to rupturing of small blood vessels, ultimately causing necrosis and sclerosis. [4]

Basic Summary

The glomeruli are the filters in the kidneys. When working normally they will move the waste, excess electrolytes, and unnecessary fluid from the bloodstream to the urine. [8] When a person develops DPGN, over 50% of the glomeruli (diffuse) become inflamed. There is also an increase in mesangial, epithelial, and endothelial (proliferative) cells. Inflammatory cells are also rapidly developed. [9] This causes damage to the kidneys and does not allow for proper filtration.[ citation needed ]

Diagnosis

The presentation of all types glomerulonephritis are the same. [4] If a patient is suspected to have DPGN, a blood and urine test will be done first. A urine test will be done to determine if there is protein or blood in the urine. A blood test will be to measure the levels of creatine in the blood. An ultrasound will be done to see if there is inflammation of the kidneys and to look for blockages.[ citation needed ]

A kidney biopsy is the most important diagnostic tool. With a biopsy, the sample will be looked at histologically. With this information, a proper diagnosis can be completed. There are many forms of glomerulonephritis, but under a microscope, DPGN will show increased cell count of polymorphonuclear cells, cellular crescents, and fibrinoid necrosis. A patient with DPGN will have more than 50% of their glomeruli involved. [4] [5] If a patient has DPGN, that means they have an active form of glomerulonephritis. [10]

Treatment

Treatment of DPGN depends on the severity of the disease. An optimal treatment for DPGN is immunosuppressive therapy. [11] Two common immunosuppressive drugs used to treat DPGN are cyclophosphamide (CYC) and mycophenolate mofetil (MMF) if the DPGN is caused by SLE. [12] CYC and MMF both preserve the renal function in patients with SLE and DPGN. [13] CYC and MMF have been known to improve proteinuria. [13] [14] There can be adverse side effects; including CYC can cause infertility in both women and men. [11] MMF has been seen to have less drug toxicity. [15] There are a variety of dosing options (oral or intravenous medications) available. [11]

If the DPGN is caused by IgA nephropathy then corticosteroids, angiotensin-converting enzyme inhibitor (ACEIs), angiotensin receptor blockers (ARBs), or both ACEIs and ARBs should be used. [15] Corticosteroids are used to suppress the immune system and to reduce inflammation. [16] ACEIs will decrease hypertension by preventing the body from creating angiotensin II, which narrows the blood vessels. ARBs block angiotensin II from acting. [17]

The patient's diet should also be changed. The patient should restrict salt intake to improve the hypertension and nephrosis. Protein restriction may reduce the progression of the disease. Fluid restriction may also be necessary if the patient is experiencing edema.

Renal corpuscle with many details including the glomerulus, glomerular capillaries, and Bowman's capsule.The glomeruli are filters in the kidneys. It is when the glomeruli become inflamed and stop filtering correctly when a person can get a type of glomerulonephritis. Renal corpuscle-en.svg
Renal corpuscle with many details including the glomerulus, glomerular capillaries, and Bowman's capsule.The glomeruli are filters in the kidneys. It is when the glomeruli become inflamed and stop filtering correctly when a person can get a type of glomerulonephritis.

[ citation needed ]

Prognosis

Prognosis is determined by the stage of the disease. [4] Aggressive therapy is recommended to avoid progressing to end-stage renal disease (ESRD), which is a strong possibility. About 10% of DPGN patients will go into ESRD. [4]

If the biopsy shows the presence of crescents, tubule-interstitial injury with inflammation atrophy and fibrosis, the outcome is worse. [4] Other factors that will influence the survival rate are the severity of proteinuria, blood urea nitrogen levels, serum creatine levels, and eGFR. Other bad prognosis features are the presence of hypertension, accelerated hematuria, and hypoalbuminemia. Males are at a higher risk factor than females. Overall, about 50% of patients with DPGN require daily dialysis within 6–12 months after disease presentation.[ citation needed ]

The percentage of glomeruli that show crescents usually correlates to the severity of the renal failure. [18] [19]

The survival rate after 5 years is about 30%. [20]

Epidemiology

DPGN prevalence varies among races. Whites are the less likely to have DPGN (12-33%); while African Americans (40-69%), Hispanics (36-61%), and Asians (47-53%) are more likely to develop it. [21]

Men are more likely to develop a more aggressive disease than women. However, women are nine times more likely to develop DPGN. [22]

DPGN occurs in all age groups, but is more prevalent in women of childbearing years. Eighty-five percent of patients develop DPGN before 55 years. [22]

End Stage Renal Disease

Research Directions

In 2014 a study was completed to diagnose glomerulonephritis based on etiology. Using immunofluorescence and light microscopy, the investigators were determining the classification for the disease based on if the disease was immune complex mediated, pauci- immune, or complement mediated. They then looked at the complement factors and immunoglobulin deposits to identify the underlying cause. The aims of this study were classifying pathophysiology and to obtain a better understanding of glomerulonephritis. [24]

Much of the research within the last 10 years has been to identify the best treatment for DPGN. Other studies about DPGN from the past 10 years has included studies for other diseases that are linked to DPGN. There are no current clinical trials for DPGN happening.[ citation needed ]

Future Studies

Activating complement pathways plays a large role in mediating inflammation. The classical pathway, lectin pathway, and alternative pathway of complement are all involved in glomerulonephritis, depending on the etiology. Inactive and active complement proteins that split fragments are found in the glomeruli. There are currently drugs available that will target the complement pathway. It has been proposed that if fluorescently tagged antibodies were used to target different split products of the complement proteins, then identification of specific pathways involved and the accumulated complement proteins in the glomeruli should be achievable. This would lead to identifying which pathways and proteins drive each type of glomerulonephritis. [10]

Related Research Articles

<span class="mw-page-title-main">Proteinuria</span> Presence of an excess of serum proteins in the urine

Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein, less than 150 mg/day; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy. Severe proteinuria can cause nephrotic syndrome in which there is worsening swelling of the body.

<span class="mw-page-title-main">Nephrotic syndrome</span> Collection of symptoms due to kidney damage

Nephrotic syndrome is a collection of symptoms due to kidney damage. This includes protein in the urine, low blood albumin levels, high blood lipids, and significant swelling. Other symptoms may include weight gain, feeling tired, and foamy urine. Complications may include blood clots, infections, and high blood pressure.

<span class="mw-page-title-main">Nephritis</span> Inflammation of the kidneys

Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules. It is one of several different types of nephropathy.

<span class="mw-page-title-main">Kidney disease</span> Damage to or disease of a kidney

Kidney disease, or renal disease, technically referred to as nephropathy, is damage to or disease of a kidney. Nephritis is an inflammatory kidney disease and has several types according to the location of the inflammation. Inflammation can be diagnosed by blood tests. Nephrosis is non-inflammatory kidney disease. Nephritis and nephrosis can give rise to nephritic syndrome and nephrotic syndrome respectively. Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.

<span class="mw-page-title-main">IgA nephropathy</span> Disease of the kidney

IgA nephropathy (IgAN), also known as Berger's disease, or synpharyngitic glomerulonephritis, is a disease of the kidney and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. Aggressive Berger's disease can attack other major organs, such as the liver, skin and heart.

<span class="mw-page-title-main">Henoch–Schönlein purpura</span> Medical condition

Henoch–Schönlein purpura (HSP), also known as IgA vasculitis, is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura, often with joint pain and abdominal pain. With kidney involvement, there may be a loss of small amounts of blood and protein in the urine, but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as a throat infection.

<span class="mw-page-title-main">Glomerulonephritis</span> Term for several kidney diseases

Glomerulonephritis (GN) is a term used to refer to several kidney diseases. Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.

<span class="mw-page-title-main">Diabetic nephropathy</span> Chronic loss of kidney function

Diabetic nephropathy, also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine, rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome. Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease. It usually is slowly progressive over years.

<span class="mw-page-title-main">Lupus nephritis</span> Inflammation of the kidneys

Lupus nephritis is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the glomeruli become inflamed. Since it is a result of SLE, this type of glomerulonephritis is said to be secondary, and has a different pattern and outcome from conditions with a primary cause originating in the kidney. The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy. On urinalysis, a nephritic picture is found and red blood cell casts, red blood cells and proteinuria is found.

<span class="mw-page-title-main">Membranous glomerulonephritis</span> Medical condition

Membranous glomerulonephritis (MGN) is a slowly progressive disease of the kidney affecting mostly people between ages of 30 and 50 years, usually white people.

<span class="mw-page-title-main">Nephritic syndrome</span> Medical condition

Nephritic syndrome is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in the glomerulus, where it is called glomerulonephritis. Glomerulonephritis is characterized by inflammation and thinning of the glomerular basement membrane and the occurrence of small pores in the podocytes of the glomerulus. These pores become large enough to permit both proteins and red blood cells to pass into the urine. By contrast, nephrotic syndrome is characterized by proteinuria and a constellation of other symptoms that specifically do not include hematuria. Nephritic syndrome, like nephrotic syndrome, may involve low level of albumin in the blood due to the protein albumin moving from the blood to the urine.

<span class="mw-page-title-main">Acute proliferative glomerulonephritis</span> Medical condition

Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). It can be a risk factor for future albuminuria. In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used. Acute glomerulonephritis resulted in 19,000 deaths in 2013, down from 24,000 deaths in 1990 worldwide.

<span class="mw-page-title-main">Rapidly progressive glomerulonephritis</span> Medical condition

Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney function, with glomerular crescent formation seen in at least 50% or 75% of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute kidney failure and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents.

<span class="mw-page-title-main">Membranoproliferative glomerulonephritis</span> Medical condition

Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane (GBM) thickening, activating the complement system and damaging the glomeruli.

<span class="mw-page-title-main">Mesangial proliferative glomerulonephritis</span> Medical condition

Mesangial proliferative glomerulonephritis (MesPGN) is a morphological pattern characterized by a numerical increase in mesangial cells and expansion of the extracellular matrix within the mesangium of the glomerulus. The increase in the number of mesangial cells can be diffuse or local and immunoglobulin and/or complement deposition can also occur. MesPGN is associated with a variety of disease processes affecting the glomerulus, though can be idiopathic. The clinical presentation of MesPGN usually consists of hematuria or nephrotic syndrome. Treatment is often consistent with the histologic pattern of and/or disease process contributing to mesangial proliferative glomerulonephritis, and usually involves some form of immunosuppressant.

Glomerulonephrosis is a non-inflammatory disease of the kidney (nephrosis) presenting primarily in the glomerulus as nephrotic syndrome. The nephron is the functional unit of the kidney and it contains the glomerulus, which acts as a filter for blood to retain proteins and blood lipids. Damage to these filtration units results in important blood contents being released as waste in urine. This disease can be characterized by symptoms such as fatigue, swelling, and foamy urine, and can lead to chronic kidney disease and ultimately end-stage renal disease, as well as cardiovascular diseases. Glomerulonephrosis can present as either primary glomerulonephrosis or secondary glomerulonephrosis.

Pauci-immune vasculitis is a form of vasculitis that is associated with minimal evidence of hypersensitivity upon immunofluorescent staining for IgG. Often, this is discovered in the setting of the kidney.

<span class="mw-page-title-main">Lupus</span> Human autoimmune disease

Lupus, technically known as systemic lupus erythematosus (SLE), is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. Symptoms vary among people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. Often there are periods of illness, called flares, and periods of remission during which there are few symptoms.

Focal proliferative nephritis is a type of glomerulonephritis seen in 20% to 35% of cases of lupus nephritis, classified as type III. As the name suggests, lesions are seen in less than half of the glomeruli. Typically, one or two foci within an otherwise normal glomerulus show swelling and proliferation of endothelial and mesangial cells, infiltration by neutrophils, and/or fibrinoid deposits with capillary thrombi. Focal glomerulonephritis is usually associated with only mild microscopic hematuria and proteinuria; a transition to a more diffuse form of renal involvement is associated with more severe disease.

Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction. Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

References

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  23. ↑ "Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2017;7:1–59". Kidney International Supplements. 7 (3): e1. December 2017. doi: 10.1016/j.kisu.2017.10.001 . ISSN   2157-1716. PMC   6341011 . PMID   30681074. S2CID   58992243.
  24. ↑ Sethi, Sanjeev (April 2014). "Etiology-Based Diagnostic Approach to Proliferative Glomerulonephritis". American Journal of Kidney Diseases. 63 (4): 561–566. doi:10.1053/j.ajkd.2013.11.019. ISSN   0272-6386. PMID   24387793.
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