Membranous glomerulonephritis history and symptoms

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

The majority of patients with [disease name] are asymptomatic.

OR

The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].

History and Symptoms

History

Common Symptoms

  • The most frequent presentation is proteinuria in nephrotic range, with or without the other findings of the complete NS. In a variable percentage of cases present as asymptomatic proteinuria. There is microscopic hematuria in most of patients, but macrohematuria is rare. Exceptionally it can appear with isolated hematuria. The renal function can be slightly altered at the time of the diagnosis in many cases, but renal failure is unusual at presentation. In 25-33% of the cases systemic hypertension is documented. MGN may appear to any age, with predilection by 4º and 5º decades of the life.
  • The clinical course of MGN is very variable, in many patients there is a favorable course; approximately 25% of patients will have partial or complete spontaneous remission, although, until 29% of them will present recurrence. Around 50% of patients will not present alteration of the renal function. In a small number of cases there will be a fast loss of renal function or death. This variable evolution makes difficult interpretation of clinical trials or treatment response. Treatment with steroids, clorambucil or other immunosuppressors has shown contradictory results; it does not exist at the present moment an universally accepted treatment.
  • Cases of post-transplant recurrent MGN have been informed, but, there are no large series that allow determining with precision the percentage of post-transplant recurrence. Since renal transplant receptors are susceptible to many causes of secondary MGN, an underlying or associated cause must be looked for. Histologically is not possible to differentiate between recurrent MGN and de novo MGN in a transplanted kidney; for this differentiation the histologic study in the native kidney is indispensable.
  • The amount of proteinuria is variable, ranging from subnephrotic to more than 20 g/day. Proteinuria is typically present for several months prior to the diagnosis of MN by renal biopsy, which highlights the more gradual development of this disease process. Other common abnormalities on urinalysis and urine microscopy include oval fat bodies, lipid droplets, and fatty casts. Microscopic hematuria occurs in up to 50 percent, but red blood cell casts are rare [113].
  • Glucosuria in the presence of normal blood glucose levels is common in patients with nephrotic syndrome, probably a consequence of tubular dysfunction from the heavy albuminuria.
  • Hypoalbuminemia and severe hyperlipidemia are almost always present at diagnosis in patients with the nephrotic syndrome but usually not in patients with subnephrotic proteinuria.
  • Approximately 70 percent of patients have normal blood pressure and glomerular filtration rate (GFR) at presentation. Acute kidney injury (AKI) is uncommon and may be due to hypovolemia due to aggressive diuresis, acute interstitial nephritis due to diuretics or other offending drugs, superimposed crescentic glomerulonephritis (which is associated with an active sediment), or, rarely, from acute renal vein thrombosis leading to renal infarction.
  • The usual course of patients with MN is either spontaneous or treatment-induced complete or partial remission or persistent nephrotic syndrome with or without slow progression to end-stage renal disease (figure 2). The prognosis of MN is discussed separately.
  • Patients with subnephrotic proteinuria have a benign long-term prognosis as long as they remain subnephrotic (less than 3.5 to 4.0 g/day). However, these patients require long-term monitoring of protein excretion since many progress to nephrotic-range proteinuria with its associated higher rate of progressive disease. The rationale for prolonged monitoring was provided by a review of 395 patients with MN, 108 of whom (27 percent) presented with subnephrotic proteinuria (less than 3.5 g/day) [130]. Among these patients, 66 (61 percent) progressed to nephrotic syndrome, 20 after the first year including 9 after more than four years.

References

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