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 (yielding proteinuria and hematuria, respectively). By contrast, nephrotic
syndrome is characterized by proteinuria and a constellation of other symptoms that specifically do
not include hematuria.[6] 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.[7]

Historically, nephritic syndrome has been characterized by blood in the urine (hematuria), high blood
pressure (hypertension), decreased urine output <400 ml/day (oliguria), red blood cell casts, pyuria,
and mild to moderate proteinuria.[8][9] If the condition is allowed to progress without treatment, it can
eventually lead to azotemia and uremic symptoms.[9] This constellation of symptoms contrasts with
the classical presentation of nephrotic syndrome (excessive proteinuria >3.5 g/day, low plasma
albumin levels (hypoalbuminemia) <3 g/L, generalized edema, and hyperlipidemia).[8][10]
Signs and symptoms that are consistent with nephritic syndrome include:

 Hematuria (red blood cells in the urine)[11]

 Proteinuria (protein in the urine) ranging from sub-nephrotic (<3.5 g/day) to >10 g/day,
[7]
 although it is rarely above nephrotic range proteinuria levels.[12]
 Hypertension[13] resting blood pressure is persistently at or above 130/80 or 140/90
mmHg.[14]
 Blurred vision[4]
 Azotemia (increased plasma Urea and Creatinine)[2]
 Oliguria (low urine output <400 ml/day)[2]
 Red blood cell casts (seen with urine analysis and microscopy)[15]
 Pyuria (white blood cells or pus in the urine)[15]

Children/adolescents[edit]
 IgA nephropathy (Note: Contrast time of onset with Post-streptococcal
Glomerulonephritis) - Most commonly diagnosed in children who recently had an upper
respiratory tract infection (URI). Symptoms typically present within 1–2 days of a non-
specific URI with severe flank/abdominal pain, gross hematuria (characterized by dark
brown or red colored urine), and edema of the hands, feet, and/or face.[16]
 Post-streptococcal glomerulonephritis (PSGN) - Similar to IgA nephropathy, post-
streptococcal glomerulonephritis (PSGN) most often occurs in children who have
recently had an upper respiratory infection (URI). In contrast with IgA nephropathy,
however, PSGN typically presents 2–3 weeks after recovering from an URI that was
caused specifically by a Streptococcus bacteria.[17] The symptoms at onset are very
similar to IgA nephropathy and include abdominal pain, hematuria, edema, and oliguria.
[18]

 Henoch–Schönlein purpura (HSP) - Often considered a systemic form of IgA

nephropathy, Henoch-Schönlein purpura (HSP) is a systemic small-vessel vasculitis that
is characterized by deposition of IgA antibody immune complexes in different key areas
throughout the body. Most often, the condition presents in children with palpable
purpura, abdominal pain, and arthritis. When the kidneys are affected, the IgA immune
 complexes deposit in the glomerulus very similarly to IgA nephropathy and will present in
a similar way.[19]
 Hemolytic uremic syndrome - Most cases occur immediately following infectious
diarrhea caused by a specific type of E. coli (O157:H7). The bacteria produces
a toxin that causes widespread inflammation and numerous blood clots in small blood
vessels (thrombotic microangiopathy). When the inflammation reaches the kidney, or the
by-products of systemic inflammation build up in the kidney, the patient will begin
showing signs of nephritic syndrome or potentially acute kidney
failure (elevated creatinine, BUN, etc).[20]
Adults[edit]
 Goodpasture syndrome - This is a rare autoimmune disease where autoantibodies are
produced that target the glomerular basement membrane in both the lungs and
the kidneys. The damage to the basement membrane causes bleeding, and the disease
often presents in patients as hematuria and hematemesis (bloody vomit). If not treated
promptly with plasmapharesis to remove the autoantibodies, it can lead to permanent
damage in the lungs/kidneys.[21]
 Systemic Lupus Erythematosus (SLE) - Better known as simply "Lupus", this
autoimmune disease can affect nearly every major system in the human body and the
kidneys are no exception. Autoantibodies produced in SLE can form immune
complexes that deposit along the glomerular basement membrane and cause
glomerular inflammation which leads to a nephritic syndrome.[22]
 Rapidly progressive glomerulonephritis - This is a syndrome of the kidney that is
characterized by rapid loss of kidney function (usually >50% decline in glomerular
filtration rate (GFR) within 3 months)[23] with glomerular crescent formation frequently
seen on kidney biopsy. Without treatment, it will quickly lead to kidney failure and
potentially death within months. This syndrome has numerous underlying causes that
can also cause nephritic syndrome, so this may be more of an association than a cause.
[24]

 Infective endocarditis - Infection that affects the inner lining of the heart (endocardium)
and can potentially cause a thrombus to form on one or more heart valves and, if left
untreated, can cause septic emboli that can have many systemic effects, including
deposition into the glomerulus, causing glomerulonephritis and nephritic syndrome.[25]
 Cryoglobulinemia - Antibodies that are sensitive to the cold can become activated in cold
conditions and cause an increase in blood viscosity (hyperviscosity syndrome) as well as
forming immune complexes that can deposit in the small blood vessels and can cause
nephritic syndrome when this occurs in the kidneys.[26]
 Membranoproliferative glomerulonephritis (MPGN) - Another type
of glomerulonephritis that is caused primarily by immune complex deposition in
the glomerular mesangium and glomerular basement membrane thickening, which
activates the complement cascade and damages the glomerulus. This damage leads to
inflammation in the glomerulus and can present with a nephritic syndrome.[27]
 Other ANCA small-vessel vasculitides - The conditions included in this category
are eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis,
and granulomatosis with polyangiitis.[9]