Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic glomerulonephritis. The condition is characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the glomerular filtration rate (GFR) and retention of uremic toxins. If disease progression is not halted with therapy, the net results are chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease. Chronic glomerulonephritis is the third leading cause of CKD, and accounting for about 10% of all patients on dialysis.
The exact cause of CKD in patients with chronic glomerulonephritis may never be known in some patients. Therefore, it has generally been accepted that the diagnosis of CKD can be made without knowledge of the specific cause. 
The National Kidney Foundation (NKF) defines CKD on the basis of either of the following:
Evidence of kidney damage based on abnormal urinalysis results (eg, proteinuria or hematuria) or structural abnormalities observed on ultrasound images
A GFR of less than 60 mL/min for 3 or more months
In accordance with this definition, the NKF developed guidelines that classify the progression of renal disease into five stages, from kidney disease with a preserved GFR to end-stage kidney failure. This classification includes treatment strategies for each progressive level, as follows:
Stage 1 – This stage is characterized by kidney damage with a normal GFR (≥ 90 mL/min); the action plan consists of diagnosis and treatment, treatment of comorbid conditions, slowing of the progressing of kidney disease, and reduction of cardiovascular disease risks
Stage 2 – This stage is characterized by kidney damage with a mild decrease in the GFR (60-90 mL/min); the action plan is estimation of the progression of kidney disease
Stage 3 – This stage is characterized by a moderately decreased GFR (to 30-59 mL/min); the action plan consists of evaluation and treatment of complications
Stage 4 – This stage is characterized by a severe decrease in the GFR (to 15-29 mL/min); the action plan is preparation for renal replacement therapy
Stage 5 – This stage is characterized by kidney failure; the action plan is kidney replacement if the patient is uremic
At the later stages of glomerular injury, the kidney are small and contracted and biopsy results cannot help distinguish the primary disease. Histology and clues to the etiology are often derived from other systemic diseases (if present). Considerable cause-specific variability is observed in the rate at which acute glomerulonephritis progresses to chronic glomerulonephritis.
The prognosis depends on the type of chronic glomerulonephritis (see Etiology). ESRD and death are common outcomes unless renal replacement therapy is instituted.
Reduction in nephron mass from the initial injury reduces the GFR. This reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of the remaining nephrons, thus minimizing the functional consequences of nephron loss. The changes, however, are ultimately detrimental because they lead to glomerulosclerosis and further nephron loss.
In early renal disease (stages 1-3), a substantial decline in the GFR may lead to only slight increases in serum creatinine levels. Azotemia (ie, a rise in blood urea nitrogen [BUN] and serum creatinine levels) is apparent when the GFR decreases to less than 60-70 mL/min. In addition to a rise in BUN and creatinine levels, the substantial reduction in the GFR results in the following:
Decreased production of erythropoietin, thus resulting in anemia
Decreased production of vitamin D, resulting in hypocalcemia, secondary hyperparathyroidism, hyperphosphatemia, and renal osteodystrophy
Reduction in acid, potassium, salt, and water excretion, resulting in acidosis, hyperkalemia, hypertension, and edema
Platelet dysfunction, leading to increased bleeding tendencies
Accumulation of toxic waste products (uremic toxins) affects virtually all organ systems. Azotemia occurring with the signs and symptoms listed above is known as uremia. Uremia occurs at a GFR of approximately 10 mL/min. Some of these toxins (eg, BUN, creatinine, phenols, and guanidines) have been identified, but none has been found to be responsible for all the symptoms.
The progression from acute glomerulonephritis to chronic glomerulonephritis is variable, depending to a considerable extent on the cause of the condition. Whereas complete recovery of renal function is the rule for patients with poststreptococcal glomerulonephritis, several other glomerulonephritides, such as immunoglobulin A (IgA) nephropathy, often have a relatively benign course, and many do not progress to ESRD. Progression patterns may be summarized as follows:
Focal segmental glomerulosclerosis – About 80% of patients progress to ESRD in 10 years; patients with the collapsing variant (malignant focal segmental glomerulosclerosis) have a more rapid progression; this form may be idiopathic or related to HIV infection
Membranous nephropathy – About 20-30% of patients with membranous nephropathy progress to chronic renal failure (CRF) and ESRD in 10 years
Poststreptococcal glomerulonephritis – About 1-2% of patients with poststreptococcal glomerulonephritis progress to CRF and ESRD; older children who present with crescentic glomerulonephritis are at greatest risk
Lupus nephritis – Overall, about 20% of patients with lupus nephritis progress to CRF and ESRD in 10 years; however, patients with certain histologic variants (eg, class IV) may have a more rapid decline.  The presence of antineutrophil cytoplasmic antibody (ANCA) is also an independent risk factor for poor renal outcomes. 
In the United States, chronic glomerulonephritis is the third leading cause of ESRD and accounts for 10% of patients on dialysis.
In Japan and some Asian countries, chronic glomerulonephritis has accounted for as many as 40% of patients on dialysis; however, subsequent data suggest that in Japan, for instance, the rate of chronic glomerulonephritis in patients on dialysis is 28%. [7, 8] The cause of this declining rate is not known. Concurrent with the decline in chronic glomerulonephritis in these countries is an increase in diabetic nephropathy in up to 40% of patients on dialysis.
Dietary education is paramount in managing patients with CKD. The typical dietary restriction is to 2 g of sodium, 2 g of potassium, and 40-60 g of protein a day. Additional restrictions may apply for diabetes, hyperlipidemia, and fluid overload.
Patients should be educated regarding the types of ESRD therapy. The specific choices of ESRD therapy include hemodialysis, peritoneal dialysis, and renal transplantation. For further information, see Mayo Clinic - Kidney Transplant Information.
Patients opting for hemodialysis should be educated on home hemodialysis (in which patients are trained to do their dialysis at home) and center hemodialysis (in which patients come to a center 3 times a week for 3.5- to 4-hour dialysis sessions). They should also be educated on the types of vascular access. Arteriovenous fistulae should be created when the GFR falls below 25 mL/min or the serum creatinine level is greater than 4 mg/dL to allow maturation of the access before the initiation of dialysis.
In the United States and most developed countries, patients on dialysis can travel. In fact, there are even dialysis cruises. However, patients should inform their social workers to make the necessary arrangements beforehand to ensure that the destination has the right resources to continue dialysis.
Sexual dysfunction and loss of libido are common in patients with kidney disease, especially men. Patients should be instructed to seek medical therapy if they experience these symptoms.
Renal failure and hypertension worsen during pregnancy in patients with CKD, particularly when the serum creatinine level exceeds 2 mg/dL, and this leads to decreased fetal viability and increased maternal morbidity in pregnant women with CKD. Therefore, women with CKD should consult their doctors before becoming pregnant. [9, 10]
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