The glomerulus is a histologically complex structure consisting of the epithelial cells (podocytes), basement membrane, capillary endothelium, and mesangium. A variety of different insults can occur within these structures causing different patterns of injury. Examples of injuries that can affect any or all of the constituents of the glomerulus are (1) overwork injury, as in CKD; (2) an inflammatory process, such as SLE; (3) a podocyte protein mutation, as in hereditary focal segmental glomerulosclerosis (FSGS); or (4) a deposition disease, as in diabetes or amyloidosis. Different glomerular patterns of injury tend to cause different clinical syndromes or findings, which may help narrow the differential diagnosis; however, when a glomerular disease is suspected, a kidney biopsy may be needed to confirm the diagnosis.
Glomerular diseases are typically classified as either nephritic or nephrotic (Figure 24–4); these are clinically differentiated according to the degree of proteinuria present. Differentiation is important because it helps narrow the differential diagnosis of the underlying glomerular disease (Table 24–8) (Table 24–9).
Glomerular diseases present within one of the clinical spectra shown; the exact presentation is determined by the severity of the underlying disease and the pattern of injury. Nephritic diseases are characterized by the presence of an active urine sediment with glomerular hematuria and often with proteinuria. Nephrotic spectrum diseases are proteinuric with bland urine sediments (no cells or cellular casts). All glomerular diseases may progress to a chronic, scarred state. (Reproduced with permission from Megan Troxell, MD, PhD.)
Table 24–8.Classification and findings in glomerulonephritis: nephritic spectrum presentations. ||Download (.pdf) Table 24–8. Classification and findings in glomerulonephritis: nephritic spectrum presentations.
| ||Typical Presentation ||Association/Notes ||Serology |
|Postinfectious glomerulonephritis ||Children: abrupt onset of nephritic syndrome and AKI but can present anywhere in nephritic spectrum ||Streptococci, other bacterial infections (eg, staphylococci, endocarditis, shunt infections) ||Rising ASO titers, low complement levels |
|IgA nephropathy (Berger disease) and Henoch-Schönlein purpura, systemic IgA vasculitis ||Classically: gross hematuria with respiratory tract infection, but can present anywhere in nephritic spectrum; Henoch-Schönlein purpura with vasculitic rash and GI hemorrhage || |
Abnormal IgA glycosylation in both primary (familial predisposition) and secondary disease (associated with cirrhosis, HIV, celiac disease)
Henoch-Schönlein purpura in children after an inciting infection
|No serologic tests helpful; complement levels are normal |
|Pauci-immune (granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, polyarteritis, idiopathic crescentic glomerulonephritis) ||Classically: crescentic or RPGN, but can present anywhere in nephritic spectrum; may have respiratory tract/sinus symptoms in granulomatosis with polyangiitis ||May be related to COVID-19, medication, or environmental exposures. ||ANCAs: MPO or PR3 titers high; complement levels normal |
|Anti-GBM glomerulonephritis; Goodpasture syndrome ||Classically: crescentic or RPGN, but can present anywhere in nephritic spectrum; pulmonary hemorrhage in Goodpasture syndrome ||May develop as a result of respiratory irritant exposure (chemicals or tobacco use) ||Anti-GBM antibody titers high; complement levels normal |