Chronic glomerulonephritis denotes a progressive deterioration of kidney function and is one of the main factors involved in the pathogenesis of chronic kidney disease (CKD) [1] [2]. It may be defined as a persistent and long-lasting inflammatory disorder of the glomeruli and is almost universally a complication of acute glomerulonephritis, distinguished by a slower progression and a milder clinical presentation [2]. A broad classification of ailments that cause glomerulonephritis can be mainly based on the two clinical syndromes produced by these etiologies [1] [2] [3] [4] [5]:

• Nephritic syndrome - Oliguria (reduced urine output), macroscopic hematuria (tea-colored urine), and hypertension are clinical hallmarks of nephritic syndrome, which typically develops due to an ongoing immunological process, thus it may be seen in both acute and chronic glomerulonephritis [1] [2]. Intrinsic renal diseases that induce this syndrome are poststreptococcal glomerulonephritis (PSGN), anti-glomerular basement membrane (anti-GBM) disease, but also immunoglobulin A (IgA) nephropathy (known as Buerger's disease), regarded as the most common etiology of glomerulonephritis in the world [1] [4]. Focal segmental glomerulosclerosis (FSGS), membranoproliferative GN, and IgA nephropathy are particularly associated with hypertension [5] [6]. In addition, systemic lupus erythematosus (SLE) and anti-neutrophil cytoplasmic antibody (ANCA) vasculitis are notable systemic causes [1] [2].
• Nephrotic syndrome - Contrary to the nephritic syndrome, minimal or no inflammation is present and marked impairment of the glomerular capacity to perform the process of filtration is the main pathological event [1]. Profound proteinuria (>3.5 g/day) resulting in hypoalbuminemia and consequent edema are prominent symptoms, whereas hypertension and vascular abnormalities are absent in the initial stages of the illness [1] [3]. However, intrinsic disorder of the kidney that causes nephritic syndrome may also induce nephrotic syndrome, such as FSGS and IgA nephropathy, while minimal change disease (MCD), diabetic nephropathy, systemic disorders (amyloidosis, SLE), and several other entities have been described in the pathogenesis of nephrotic syndrome [1] [2] [3].

• Periodontitis

  Furthermore, the dental and periodontal health of the patients undergoing HD for CGN was comparable to that of the controls. [ncbi.nlm.nih.gov]

• Hypertension

  The prevalence of hypertension was 42%. [ncbi.nlm.nih.gov]

  Focal segmental glomerulosclerosis (FSGS), membranoproliferative GN, and IgA nephropathy are particularly associated with hypertension. [symptoma.com]

• Amenorrhea

  A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. [ncbi.nlm.nih.gov]

The diagnosis of chronic glomerulonephritis may be difficult to make in its initial stages due to an asymptomatic or milder clinical course [2], which is why a thorough workup is imperative. The physician must obtain a detailed patient history that will address the appearance of macroscopic hematuria, hypertension, or peripheral edema. History of drug use is essential during the interview since non-steroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, and penicillamine (a chelating agent) have been listed as iatrogenic causes of glomerulonephritis [1]. Infections are an important etiology of glomerulonephritis as well, such as viral hepatitis (B and C), human immunodeficiency virus (HIV) infection, and many other bacterial/viral/fungal pathogens [1] [2], which is why the presence of additional symptoms must be assessed. Laboratory studies, however, are crucial for diagnosing chronic glomerulonephritis. Evaluation of serum electrolytes and creatinine, together with urinalysis for hematuria and protein content are key steps for identifying renal function abnormalities [1] [2]. The role of urinalysis is further strengthened by the fact that a significant number of patients are asymptomatic when microscopic hematuria is detected [7]. The glomerular filtration rate (GFR), considered to be the main indicator of renal function, can be calculated based on either serum creatinine levels (together with other components required for the calculation, such as age and gender) [1] [8]. A full immunological workup (antinuclear antibody test, antineutrophil cytoplasmic antibodies test, anti-double-stranded DNA test, complement component 3 exam), ultrasonography, and eventually a renal biopsy might be necessary in order to confirm the underlying cause of chronic glomerulonephritis [1] [2].

• Bilateral Small Kidneys

  small kidneys Microscopic (histologic) description Glomerulosclerosis, tubular atrophy and thyroidization, interstitial fibrosis and lymphocytic inflammation Arterial and arteriolar sclerosis Microscopic (histologic) images Images hosted on other servers [pathologyoutlines.com]

• Small Kidney

  kidneys with thin granular cortex and increased peripelvic fat Gross images Images hosted on other servers: Due to hypertension Chronic glomerulonephritis Bilaterally small kidneys Microscopic (histologic) description Glomerulosclerosis, tubular atrophy [pathologyoutlines.com]

• Creatinine Increased

  Some authors have found that persistent hypertension, serum creatinine increase at diagnosis, and macroscopic hematuria episodes are also related to worse prognosis. [kidneypathology.com]

• Amino Acids Increased

  Most amino acids increased two- or threefold. [ncbi.nlm.nih.gov]

• Glucagon Increased

  ANP and glucagon increased equally in both groups. Most amino acids increased two- or threefold. [ncbi.nlm.nih.gov]

1. Isbel NM. Glomerulonephritis--management in general practice. Aust Fam Physician. 2005;34(11):907-913.
2. Porter RS, Kaplan JL. Merck Manual of Diagnosis and Therapy. 19th Edition. Merck Sharp & Dohme Corp. Whitehouse Station, N.J; 2011.
3. Lewis G, Maxwell AP. Timely diagnosis and treatment essential in glomerulonephritis. Practitioner. 2015;259(1779):13-7, 2.
4. Kawasaki Y. Mechanism of onset and exacerbation of chronic glomerulonephritis and its treatment. Pediatr Int. 2011;53(6):795-806.
5. Sethi S, Nester CM, Smith RJH. Membranoproliferative Glomerulonephritis and C3 Glomerulopathy: Resolving the Confusion. Kidney Int. 2012;81(5):434-441.
6. Ihm C-G. Hypertension in Chronic Glomerulonephritis. Electrolyte Blood Press. 2015;13(2):41-45.
7. Chadban SJ, Briganti EM, Kerr PG, et al. Prevalence of kidney damage in Australian adults: the AusDiab kidney study. J Am Soc Nephrol. 2003;14:S131–138.
8. Levey AS, Eckardt KU, Tsukamoto Y, et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2005 Jun;67(6):2089-100.