Overview Nephritic syndrome is one of two clinical patterns seen in glomerular disease. Nephritic Syndrome is characterised by haematuria, proteinuria, hypertension and oligouria. Nephritic syndrome can be further classified based on light microscopic features:
Definition Glomerular Disease: Disease effecting the glomerulus. Glomerular disease reduces the ability of the kidneys to maintain a balance of certain substances in bloodstream Nephritic Syndrome: Group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney, or glomerulonephritis. Nephrotic Syndrome: kidney disease, especially when characterized by oedema and the loss of protein from the plasma into the urine due to increased glomerular permeability Acute Kidney Injury: Characterized by abrupt deterioration in kidney function, manifested by an increase in serum creatinine level with or without reduced urine output. The spectrum of injury ranges from mild to advanced, sometimes requiring renal replacement therapy. The diagnostic evaluation can be used to classify acute kidney injury as prerenal, intrinsic renal, or postrenal. Chronic Kidney Failure: Defined as the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated glomerular filtration rate (GFR), that persists for more than three months |
The page will focus on four common nephritic syndromes towards the end:
The kidneys are retroperitoneal organs (at the back of abdomen) and lies between T11 and L3, the left kidney lying slightly higher than the right kidney.
The kidney is surrounding by an outer membrane called the renal capsule. The outer layer of the kidney is the renal cortex where most of the nephrons are situated. The inner layer is the renal medulla which contain renal pyramids. The renal pyramids drain urine into the minor - major calyces before draining to the renal pelvis then the ureter.
Arterial blood supply
The Nephrons are functional units of the kidney. There are millions of nephrons. A nephron is made up of:
The glomerulus is a network of blood vessels that are located within the bowman's capsule. To understand the cause, pathophysiology and effect of glomerulonephritis it is important to learn the layers of the glomerulus + bowman's capsule.
From inside out the layers are (as depicted in the image above):
Side note Pyuria can also be conspicuous in nephritic patients, particularly in inflammatory forms of glomerulonephritis such as poststreptococcal glomerulonephritis. However, pyuria is never the sole manifestation of nephritic urine sediment. |
To come
Overview The most common primary glomerulonephritis in the world, affecting an estimated 1.5% of the population. Often presents with haematuria in the 2nd and 3rd decades. Occurs due to IgA immune complex deposition in glomerular mesangium and capillary wall, associated complement 3 activation and IgG binding and resulting glomerular destruction. Damage results in chronic microscopic or recurrent macroscopic haematuria, often after acute URTI or gastroenteritis
Remember Previously considered relatively benign, it is now recognized that 30– 50% will progress to significant CKD over time. |
Risk Factors
Clinical Presentation
Side note Recurrent gross haematuria is the hallmark of IgA nephropathy. Closely related to IgAN is Henoch–Schönlein purpura (HSP), a condition that occur in children. HSP is a small vessel systemic vasculitis characterised by IgA deposition in affected blood vessel, with kidney biopsy findings usually indistinguishable from IgAN |
Pathology and Diagnosis
Treatment for IgA nephropathy is only required with persistent proteinuria, recurrent haematuria, mild to moderate findings on renal biopsy and evidence of decreased GFR. Isolated haematuria does not require treatment
Pharmacology Cyclophosphamide |
Complications
Prognosis
Overview Post-infectious glomerulonephritis is classically associated with streptococcal infection, but infection of almost any cause may be associated with an acute nephritic syndrome and a diffuse proliferative GN on kidney. Post-infectious glomerulonephritis is an immune complex-mediated GN that usually occurs in childhood (age <7 years) following (usually) a upper respiratory tract infection (Tonsilitis, pharyngitis) but also impetigo, otitis media and cellulitis 1-2 weeks earlier.
Clinical presentation
Side note The most common Post-infectious glomerulonephritis is Post-streptococcal glomerulonephritis. Other causes include: streptococcal pneumococcal, meningococcal, salmonella, mycobacterial, syphilis. Viruses: influenza B, mumps, rubella, coxsackie, hepatitis B, EBV, CMV. Fungi: candida, Coccidioides, Histoplasma. Parasites: malaria, filiariasis, toxoplasmosis, or schistosomiasis. |
Investigations
Pathology/Diagnosis
Course of Post-Infectious Glomerulonephritis
Treatment
Overview Renal involvement is common in systemic lupus erythematosus (SLE). There are several types of renal disease in SLE (most commonly, immune complex-mediated glomerular disease), which are usually differentiated with a renal biopsy
Pathophysiology The pattern of glomerular injury seen in systemic lupus erythematosus (SLE) (and in other immune complex-mediated glomerular diseases) is primarily related to the site of formation of the immune deposits, which are primarily due to anti-double-stranded DNA antibodies (anti-dsDNA, or anti-DNA)
Classification
Overview Anti-GBM antibody disease is a disorder in which circulating antibodies are directed against an antigen intrinsic to the glomerular basement membrane (GBM), thereby resulting in acute or rapidly progressive glomerulonephritis that is typically associated with crescent formation.
Patients with anti-GBM antibody disease usually present with rapidly progressive glomerulonephritis: acute renal failure, nephritic urine sediment, and non-nephrotic proteinuria. Pulmonary involvement (alveolar haemorrhage) is present in 40 to 60 percent of patients
Diagnosis
Other investigations