Key Clinical Signs and Symptoms of Chronic Glomerulonephritis: Early Recognition Matters

Chronic glomerulonephritis (CGN) is a progressive, immune-mediated kidney disorder that damages the glomeruli—the tiny filtering units in the kidneys. Unlike acute kidney conditions, CGN often develops silently over months or years, making early symptom awareness critical for timely diagnosis and intervention. The five hallmark clinical manifestations include hematuria, proteinuria, hypertension, edema, and progressive renal dysfunction. Recognizing these signs—and understanding their nuances—can significantly influence long-term outcomes and help prevent irreversible kidney damage.

Hematuria: A Telltale Sign of Glomerular Injury

One of the most common early indicators of chronic glomerulonephritis is hematuria—blood in the urine. This isn't always visible to the naked eye. In fact, many patients experience persistent microscopic hematuria, detectable only through urinalysis. Others may have intermittent episodes of gross hematuria, where urine appears pink, cola-colored, or smoky. When examined under a phase-contrast microscope, over 80% of red blood cells often show abnormal shapes—so-called dysmorphic RBCs—a strong clue pointing to glomerular rather than urinary tract bleeding.

Proteinuria: More Than Just a Lab Abnormality

Proteinuria in CGN typically reflects selective or partially selective loss of plasma proteins due to damaged glomerular filtration barriers. It's commonly characterized by glomerular-type proteinuria, involving medium- to high-molecular-weight proteins like albumin and immunoglobulins. In milder cases, protein excretion may range from 0.5 to 3.5 g/day. However, when daily protein loss exceeds 3.5 g—especially when accompanied by hypoalbuminemia, hyperlipidemia, and significant edema—it meets the diagnostic criteria for nephrotic syndrome. This advanced stage also increases susceptibility to infections, thromboembolic events, and accelerated renal decline.

Edema: From Facial Swelling to Systemic Fluid Retention

Fluid retention in CGN manifests in two primary patterns. The first is "nephritic edema"—typically starting around the eyes and face, especially noticeable upon waking. This results from sodium and water retention driven by reduced glomerular filtration and activation of the renin-angiotensin-aldosterone system (RAAS). The second is "nephrotic edema", which tends to be more severe and generalized—from ankles and legs up to the abdomen (ascites) and even lungs (pulmonary edema)—often linked to profound hypoalbuminemia and capillary leak. Both types signal worsening disease activity and warrant prompt clinical evaluation.

Hypertension: A Dual-Pathway Complication

Renal hypertension is not just a side effect—it's a key driver of disease progression in CGN. It arises through two interrelated mechanisms: volume overload (from sodium/water retention) and RAAS overactivation (due to ischemic kidney tissue). Uncontrolled blood pressure further injures glomeruli, creating a dangerous feedback loop. Importantly, hypertension in CGN may appear before significant changes in serum creatinine or GFR are evident—making routine BP monitoring essential in at-risk populations, including those with persistent hematuria or proteinuria.

Progressive Renal Dysfunction: From Reduced Filtration to End-Stage Disease

Left untreated or poorly managed, chronic glomerulonephritis gradually impairs the kidneys' ability to filter waste, regulate electrolytes, and produce vital hormones like erythropoietin and active vitamin D. This leads to a slow but steady decline in estimated glomerular filtration rate (eGFR). Over time, patients may develop fatigue, anemia, metabolic acidosis, and bone mineral disorders. Without intervention—including optimized blood pressure control, RAAS inhibitors, dietary modifications, and sometimes immunosuppressive therapy—the disease can advance to end-stage kidney disease (ESKD), requiring dialysis or transplantation. Early detection and multidisciplinary care dramatically improve prognosis and quality of life.