Renal scarring is a pathological process where the normal, functional tissue of the kidney is permanently replaced by stiff, non-functional material. This condition represents the final common pathway for most forms of progressive kidney damage, severely compromising the organ’s ability to perform its filtration duties. The development of this scar tissue, primarily composed of excessive protein deposits, leads to a gradual but irreversible decline in kidney function. This decline in efficiency can eventually lead to chronic kidney disease.
What Happens When Kidneys Scar?
The process of renal scarring involves the destruction of the kidney’s functional units, called nephrons, which are replaced by scar tissue. This destructive process, known as fibrosis, involves the excessive deposition of extracellular matrix proteins, most notably collagen, within the kidney’s structure. Normal kidney tissue is soft and porous, designed for filtering, but the resulting scar tissue is dense and restrictive.
This structural change impairs the kidney by disrupting the architecture of the nephrons and surrounding blood vessels. The stiff, collagenous material compresses healthy tissue and obstructs fine capillaries, reducing blood flow and filtration capacity. A central mediator in this process is transforming growth factor-beta (TGF-β), which signals resident cells to transform into myofibroblasts, the primary producers of scar-forming collagen. The result is a smaller, often irregularly shaped kidney with sections of tissue that can no longer filter blood or regulate fluid balance.
Key Conditions That Lead to Scar Formation
Renal scarring is primarily triggered by two categories: acute inflammation from infection or structural issues, and chronic damage from systemic diseases. One major pathway involves infection, specifically acute pyelonephritis, a severe bacterial infection of the upper urinary tract. Recurrent episodes of this infection, particularly in children, cause significant inflammation that injures the kidney parenchyma.
This infection-related scarring is often associated with vesicoureteral reflux (VUR), where urine flows backward from the bladder toward the kidney. VUR allows bacteria to reach the kidney easily, causing the repeated, intense inflammatory response that leads to scar formation, a condition sometimes termed reflux nephropathy. The severity of the VUR correlates with an increased risk of scar formation.
The second major cause comes from systemic diseases that damage the kidney’s vascular network. Uncontrolled high blood pressure (hypertension) strains the small filtering blood vessels within the kidney, leading to chronic injury and subsequent fibrosis. Similarly, diabetes causes high levels of glucose that damage the kidney’s filtering units, the glomeruli, triggering a fibrotic cascade. Both hypertension and diabetes initiate chronic damage that results in scar tissue accumulation.
How Renal Scarring is Detected
Diagnosing renal scarring involves a combination of imaging tests that visualize the damage and blood tests that assess the resulting loss of function. The most specific imaging test for confirming focal scarring is the Dimercaptosuccinic acid (DMSA) scan. This nuclear medicine test uses a radioactive tracer that healthy kidney tissue absorbs, but scarred or non-functional areas do not, revealing clear defects in the kidney structure.
Ultrasound is often used as an initial, non-invasive imaging tool to look at the kidney’s overall size, shape, and structure. While it can detect diffuse scarring or a significant reduction in kidney size, ultrasound has poor sensitivity for detecting small, focal scars, meaning a normal result does not rule out damage. To assess the functional impact, blood tests measure serum creatinine levels and calculate the estimated Glomerular Filtration Rate (GFR). A decreasing GFR indicates that the total filtering capacity of the remaining healthy nephrons is declining.
Slowing Down Scar Progression
Since scar tissue is permanent and cannot be reversed, management focuses on slowing the progression of further damage to preserve the remaining healthy kidney tissue. A primary strategy involves controlling the underlying systemic diseases that fuel the scarring process. For patients with high blood pressure or diabetes, maintaining strict control of blood pressure and blood sugar levels reduces ongoing injury to the kidney’s microvasculature.
Medications that block the Renin-Angiotensin-Aldosterone System (RAAS) are beneficial, specifically Angiotensin-Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs). These drugs lower overall blood pressure, reduce pressure inside the glomeruli, and decrease protein leaking into the urine, which is independently damaging to the kidney.
For scarring related to VUR in children, treatment often involves prophylactic low-dose antibiotics to prevent recurrent pyelonephritis, or surgical correction of the reflux to eliminate the structural issue. Lifestyle adjustments, such as adopting a diet low in sodium and protein and stopping smoking, also help reduce the burden on the remaining functional nephrons.