Natural course of kidney disease — The initial damage to the kidney can lead to a variety of clinical manifestations, from asymptomatic hematuria to kidney failure requiring dialysis. Many patients can recover completely, with no or only minor sequelae. For example, long-term prognosis for glomerulonephritis after streptococcal infection is most common. In contrast, some patients (such as patients with lupus nephritis) repeatedly develop chronic kidney damage, resulting in persistent damage. In addition, some patients with initial disease inactivity or cured may have progressive kidney disease due to hemodynamics and other mechanisms.
In addition to differences in individual disease activity, these differences are manifested to some extent by the way the kidney responds to injury. The kidneys can adapt to the injury by increasing the filtration rate of the residual normal nephron, a process known as adaptive hyperfiltration. Therefore, serum creatinine concentrations in patients with mild renal insufficiency are usually normal or near normal. A variety of other homeostatic mechanisms (mostly in the renal tubules) maintain serum concentrations of sodium, potassium, calcium, and phosphorus, as well as total body water levels, especially in patients with mild to moderate renal insufficiency.
Although the adaptive hyperfiltration mechanism is initially beneficial, it appears to cause long-term damage to the glomeruli of the residual nephron, manifested by proteinuria and progressive renal failure. This process appears to be the cause of initial disease inactivity or renal failure in cured patients. Estimation of single nephron glomerular filtration rate (SNGFR) in humans supports high filtration is an important pathophysiological mechanism [2]. Elevated SNGFR is associated with risk factors for disease progression, including obesity, a family history of end-stage renal disease (ESRD), and more severe glomerular sclerosis and arteriosclerosis suggesting that the remaining nephrons compensate for total GFR. Measu
