While Reviewing Urine Lab Results the Nurse Remembers the Glomerular
Mo Med. 2011 Jan-Feb; 108(1): 33–36.
Clinical Presentation & Management of Glomerular Diseases: Hematuria, Nephritic & Nephrotic Syndrome
Abstract
Because the differential diagnosis for glomerulonephritis (GN) is broad, using a classification schema is helpful to narrow the causes of GN in a systematic way. The etiology of glomerulonephritis tin can be classified by their clinical presentation (nephrotic, nephritic, chop-chop progressive GN, chronic GN) or by histopathology. GN may be restricted to the kidney (primary glomerulonephritis) or be a secondary to a systemic disease (secondary glomerulonephritis). The nephrotic syndrome is defined past the presence of heavy proteinuria (protein excretion greater than 3.0 g/24 hours), hypoalbuminemia (less than 3.0 g/dL), and peripheral edema. Hyperlipidemia and thrombotic disease may be nowadays. The nephritic syndrome is associated with hematuria and proteinuria and aberrant kidney function and carries poorer prognosis and is typically associated with hypertension. The predominant cause of the nephrotic syndrome in children is minimal change disease. The most common causes of nephritic syndrome are mail service infectious GN, IgA nephropathy and lupus nephritis. Chronic GN is slowly progressive and is associated with hypertension and gradual loss of kidney part. Treatment includes non-specific measure out aimed at controlling hypertension, edema, proteinuria and illness modifying immunosuppression.
Introduction
It is adequately common for glomerular affliction patients to be asymptomatic and during a md'south visit incidentally find aberrant urinary findings. A practiced history, physical examination and common urine investigations tin narrow down the differential diagnosis to few weather. On the other farthermost, a severely ill patient of acute glomerulonephritis (GN) could present with astute renal failure, edema, hypertension and maybe seizure, but such presentations are relatively less common. This review will focus on summarizing common, glomerular diseases management in an out-patient set up.
Clinical Presentations
The clinical presentation can vary from being asymptomatic to acutely severe illness. See Effigy i. Specific history should include questioning for early morning time periorbital puffiness and evening time lower extremities edema, foamy urine, and alter in urine color, volume and/or odor. Systemic diseases that are unremarkably associated with glomerular disease are diabetes, hypertension, lupus, vasculitis, and viral infections similar hepatitis B, C and HIV 1 , 2 , iii. A positive family history of Alport'due south syndrome in association with hearing loss, uncommon forms of familial focal segmental glomerulosclerosis (FSGS), or IgA disease is invaluable in arriving at a specific diagnosis. Certain mutual drugs are associated with glomerular illness (Run into Table 1). Several glomerulonephritis are preceded by acute streptococcal infection, infective endocarditis or viral infections. Ofttimes IgA nephropathy is brought to attending by hematuria caused by an acute systemic infection. Several malignancies are frequently associated with glomerular disease (Come across Tabular array 2). It is non uncommon for some malignancies to commencement manifest with renal bug. Physical test findings that point toward glomerular disease include dependent edema, periorbital edema, generalized anasarca, white nails, and xanthelasmas pointing nephrotic syndrome, or pulmonary signs especially hemorrhage suggestive of nephritic syndrome.
Tabular array 1
Common Drugs Known to Cause Glomerular Diseases
Minimal change illness:
|
Membranous GN:
|
Focal Segmental Glomerulosclerosis:
|
Hemolytic Uemic Syndrome:
|
Table two
Glomerular Diseases Associated with Common Malignancies
Bleary GN:
|
Minimal change disease:
|
Membrano-proliferative GN:
|
Urine examination findings are very critical in determining the management of further work upward. Frequently urine findings of hematuria, proteinuria or both may be the start sign of glomerular disease. Glomerular origin of RBCs is substantiated by findings of dysmorphic RBCs, acanthocytes, abnormal casts and proteinuria. Presence of isolated monomorphic RBCs necessitates work-up for lower urinary tract bleeding or lower urinary tract infection.
Asymptomatic Balmy Proteinuria
Normal proteinuria is less than 150 mg/day, which may comprise up to xx–xxx mg of albumin. Non-nephrotic proteinuria is defined as a urine protein excretion of less than 3.5 gm/day or a random urine protein to creatinine ratio of less than 3. Increased poly peptide excretion is a hallmark of glomerular disease. When the urine dipstick for albumin is negative while the quantitative proteinuria is excessive suggests urinary excretion of light chain proteins. Functional proteinuria is usually transient and is typically associated with exercise and transient systemic illness. Orthostatic proteinuria occurs in children and immature adults but in upright position and absent while recumbent in absence of any identifiable secondary crusade. Prognosis is uniformly skillful.
Stable asymptomatic non-nephrotic proteinuric patient with normal kidney part is managed by close observation and a kidney biopsy is usually not indicated. However, presence of microscopic hematuria in association with a proteinuria though asymptomatic does change the prognosis and requires a kidney biopsy.
Nephrotic Syndrome
Nephrotic syndrome (run into Figure 1) is usually a chronic condition and with the exception of MCD, most causes eventually lead to chronic progressive renal failure. Mutual causes of nephrotic syndrome are listed in Table 3. Nearly minimal modify diseases do reply to corticosteroids and a small-scale fraction of patients are steroid dependent. Edema in nephrotic syndrome is a combination of hypoalbuminemia and salt and water retentivity4. In some could lead to hypertension particularly in clan with aberrant kidney function. Proteinuria causes low albumin state and marked negative nitrogen residual and hyperlipidemia5. Loss of coagulation proteins lead to hypercoagulable state and increased platelet assemblage. These patients have increased gamble of venous and arterial thromboembolism6. Low poly peptide state increases risk for bacterial infection7. It is not uncommon to take acute renal failure due to book depletion, renal vein thrombosis, or adverse drug reactions.
Table 3
Common Causes of Nephrotic Syndrome
-
Minimal change affliction
-
Focal segmental glomerulosclerosis
-
Membranous GN
-
Membranoproliferative GN (Type 1 and two and associated with cryoglobinemia)
-
Daibetic nephropathy
-
Amyloid
Nephritic Syndrome
Usually a consequence of glomerular inflammation (Run into Figure 1) and is associated with reduced kidney function, non-nephrotic proteinuria, hematuria with red cell casts, hypertension and edema. A mutual mode of presentation, represented by the acute post-streptococcal GN, is oliguria, cola colored urine, weight gain, edema, and hypertension over a few days. Distinction betwixt nephrotic and nephritic syndrome is usually directly forward. Notwithstanding, some glomerular diseases particularly the MPGN can present every bit nephrotic or nephritic. Common causes of nephritic syndrome are listed in Table 4. Rapidly progressive renal failure is a hall marker of speedily progressive glomerulonephritis syndrome and presents with nephritic urine pictureviii.
Tabular array 4
Common Causes of Nephritic Syndrome
-
Post-streptococcal GN
-
Infective endocarditis
-
Shunt nephritis
-
IgA nephropathy
-
Lupus Nephritis
-
Goodpasture'southward
-
Vasculitis
Chronic Glomerulonephritis
Patients with chronic GN progresses slowly and are typically associated with hypertension, edema, chronic anemia, mild to moderate proteinuria, abnormal urine sediment, chronic renal bone illness and mild metabolic acidosis. Both kidneys gradually compress in size. Kidney biopsy may help in diagnosis and prognosis prediction, but is therapeutically low in value. Nonetheless, biopsy is indicated especially for those who are potential kidney transplant candidates.
Handling of Glomerular Disease
Focus of handling for secondary glomerular affliction is to aggressively manage the underlying systemic illness such as underlying infection. In virtually instances this approach results in resolution of GN. For primary GN the therapy consists of supportive management and disease modifying specific therapy. Supportive therapy is aimed at decision-making blood pressure, relieving edema, reduction of proteinuria and hyperlipidemia, and management of any other metabolic derangement that may exist present. In a small minority of patients, such non-specific therapies allow spontaneous resolution of GN. If successful, patients could exist spared of toxic immunosuppression medications, which have serious inevitable side effects. There are only a handful of GNs where immunosuppression and/or supportive therapy predictably results in complete remission such as minimal modify disease, post-infectious GN.
The full general principles of disease modifying immunosuppression therapy are aimed at blocking, reduction or rarely elimination of antigen furnishings. More than astringent and astute illnesses, such as apace progressive glomerulonephritis8 are the ones that have the almost do good from aggressive immunosppressive direction. On the contrary, chronic GNs are rather resistant to immunosuppression. Conditions where kidney biopsy demonstrates all-encompassing scarring, renal part is rapidly failing and is associated with anuria (urine output >200 ml/24-hour interval) should exist managed conservatively because the risk do good ratio is unfavorable. Dialysis may be given equally needed.
As about immunosuppressive protocols are non-specific in nature, patients are heavily immunosuppressed and are at run a risk for atypical infections. The major drugs that are included in most protocols are corticosteroids azathioprine and cyclophosphamide. Recently favorable results have been reported with drugs used in kidney transplant patients such every bit calcineurin inhibitors, mycophenalic acid and rapamycin.
The nephrology community is slowly experimenting drugs developed and used in oncology field, including rituximab. The literature reports of immunosuppressive therapies are hard to interpret and not easy to translate in practise due to studies that consist of small number of patients, lack of prospective randomized trials, variable nature of GNs.
Summary
Considering the differential diagnosis for GN is wide, using a classification schema is helpful to narrow the causes of GN in a systematic manner. The etiology of glomerulonephritis tin be classified by their clinical presentation (nephrotic, nephritic, rapidly progressive GN, chronic GN) or by histopathology. GN may be isolated to the kidney (chief glomerulonephritis) or exist a component of a systemic disorder (secondary glomerulonephritis).
The nephrotic syndrome is defined by the presence of heavy proteinuria (protein excretion greater than 3 1000/24 hours), hypoalbuminemia (less than 3.0 g/dL), and peripheral edema. Hyperlipidemia and thrombotic disease may be present.
The nephritic syndrome is associated with hematuria and proteinuria and abnormal kidney role and carries poorer prognosis and is typically associated with hypertension. The predominant cause of the nephrotic syndrome in children is minimal alter disease. The most common causes of nephritic syndrome are post infectious GN, IgA nephropathy and lupus nephritis.
Chronic GN is slowly progressive and is associated with hypertension and gradual loss of kidney function. Treatment includes non-specific measure aimed at controlling hypertension, edema, proteinuria and disease modifying immunosuppression.
Biography
•
Ramesh Khanna, Doctor, MSMA member since 2010, is the Karl D. Nolph, Md, Chair in Nephrology, Professor of Medicine, Manager, Segmentation of Nephrology, at the University of Missouri Schoolhouse of Medicine.
Contact: ude.iruossim.htlaeh@rannahk.
Footnotes
References
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Articles from Missouri Medicine are provided here courtesy of Missouri State Medical Association
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6188440/
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