What Causes Glomerular Disease and How Is It Treated?

The kidneys continuously filter the blood to remove waste products and maintain the body’s balance of fluids and electrolytes. This filtering takes place within millions of microscopic units called nephrons. Glomerular disease refers to conditions that attack the glomeruli, the initial, high-pressure filtering components within each nephron. When the glomeruli are damaged, they lose the ability to properly strain the blood, impairing waste removal and leading to a buildup of toxins.

How the Glomerulus Filters Waste

The glomerulus is a dense cluster of tiny blood vessels, or capillaries, encased within Bowman’s capsule. This structure is highly selective about what passes through its barrier. Blood enters the glomerulus under pressure, which drives the filtration process.

The glomerular filtration barrier consists of three specialized layers: the capillary wall, the basement membrane, and specialized cells called podocytes. This barrier permits water and small molecules, such as urea, creatinine, and excess salts, to pass out of the blood and into the capsule.

The filtration membrane retains larger, beneficial components in the bloodstream. Large proteins, such as albumin, and all blood cells are normally blocked from crossing the barrier due to their size and electrical charge. After filtration, the resulting fluid moves into the renal tubules where the body reabsorbs most water and necessary nutrients before the remaining waste is excreted as urine.

Drivers of Glomerular Damage

Glomerular diseases are broadly categorized based on whether the condition originates within the kidney itself (primary) or is a consequence of a disease affecting the entire body (secondary). This distinction dictates the management strategy.

Primary glomerular diseases are those that attack the glomeruli directly, often involving an autoimmune response where the body’s immune system mistakenly targets the kidney tissue. Examples include IgA nephropathy, where an antibody called immunoglobulin A deposits in the glomeruli, and Focal Segmental Glomerulosclerosis (FSGS), which involves scarring in sections of the glomeruli. Minimal change disease is another primary form that is often seen in children.

Secondary glomerular diseases result from systemic conditions that cause widespread damage, with the glomeruli being one of the affected sites. The most common drivers globally are uncontrolled diabetes and high blood pressure.

In diabetic kidney disease, high blood glucose levels over time damage the glomeruli, leading to thickening and scarring. Chronically high blood pressure similarly strains the blood vessels of the glomeruli, causing wear and tear that impairs filtration. Other secondary causes include systemic autoimmune diseases, such as lupus nephritis, where autoantibodies accumulate in the glomeruli and cause inflammation.

Physical Signs of Kidney Trouble

When the glomerular filter is compromised, signs often relate to substances abnormally leaking out of the blood or being retained in the body. One common sign is proteinuria, the presence of excessive protein in the urine.

Since the damaged filter can no longer retain large proteins like albumin, they spill into the urine, which frequently results in foamy urine. Another common finding is hematuria, or blood in the urine, which may be visible as pink, red, or cola-colored, but is often only detectable under a microscope.

The loss of protein from the blood significantly reduces the blood’s ability to hold fluid in the vessels, causing fluid to leak into surrounding tissues. This results in edema, which is swelling that is most noticeable in the legs, ankles, and around the eyes.

High blood pressure is both a potential cause and a common consequence of glomerular damage, as the kidneys play a major role in regulating blood pressure. Patients may also experience generalized symptoms, such as fatigue and loss of appetite, due to the progressive buildup of waste products in the blood.

Identifying and Treating Glomerular Disease

Diagnosis begins with routine screening tests, often prompted by the discovery of protein or blood in the urine during a urinalysis. Blood tests are used to measure waste products like creatinine and calculate the estimated glomerular filtration rate (eGFR), which indicates how efficiently the kidneys are filtering.

While initial tests reveal a problem, the definitive step to classify the specific type of glomerular disease is often a kidney biopsy. This procedure uses a specialized needle to remove a tissue sample, which is examined under a microscope to identify the exact pattern and cause of the damage. A precise diagnosis is necessary because treatment strategies vary significantly based on the underlying cause.

Treatment focuses on slowing the progression of kidney damage and managing underlying systemic conditions. For secondary diseases, this means strict control of blood sugar in diabetic patients and management of high blood pressure.

Medications called Angiotensin-Converting Enzyme (ACE) inhibitors or Angiotensin Receptor Blockers (ARBs) are often prescribed. They lower blood pressure and reduce pressure within the glomeruli, which helps decrease protein leakage.

For primary glomerular diseases driven by autoimmune activity, treatment involves immunosuppressive medications, such as steroids or other immune-modulating drugs. Lifestyle adjustments are also important and include dietary changes to limit sodium, protein, and sometimes potassium and phosphorus, depending on the disease stage, to reduce the workload on the kidneys.