Introduction:
Mycobacterium leprae is the cause of leprosy. This chronic illness can sometimes involve the entire body and be extremely debilitating. All forms of the disease have been reported to involve the kidneys, with multibacillary forms reporting a higher frequency of involvement. The way that the bacilli present clinically varies depending on how the host immune system responds to them. There are ‘reactional states’ during the course of the illness, where the immune system attacks the bacilli and exacerbates the clinical symptoms.
What Is Leprosy Nephropathy?
Necropsy investigations revealed tubulointerstitial lesions and glomerulonephritis at the start of the twentieth century. These findings provided the first description of renal involvement in leprosy. Acute and chronic glomerulonephritis, interstitial nephritis, secondary amyloidosis (amyloids build up in organs and tissues), and pyelonephritis are among the various renal lesions associated with leprosy that have been found.
What Causes Leprosy Nephropathy?
The way glomerulonephritis happens in leprosy is not entirely clear. It is possible that the leprosy bacteria (M. leprae) directly cause kidney damage because they've been found in the kidney's filtering units (glomeruli) of infected patients. The kidney damage is likely due to the body's immune response, where there's a decrease in complement and the formation of immune complexes in the glomerular area. These immune complexes are found in various parts of the kidney structure when looked at under a special microscope. Some studies have also noted increased cell growth in the kidney's supporting structure (mesangial proliferation) and the presence of a type of antibody (immunoglobulin A) in that area.
Certain studies have reported a consistent correlation between kidney disease, lepromatous form of leprosy, and erythema nodosum. Leprosy nephropathy can manifest in various forms and without the reactional state, though it is more common in the multibacillary form. Reactional state, multibacillary (higher bacterial load) classification, and advanced age were risk factors for kidney damage.
What Are the Clinical Findings of Leprosy Nephropathy?
In people with leprosy, certain changes may be seen in their urine. Bleeding in the urine (hematuria) is more common in the Virchowian form of leprosy and during a specific skin condition called erythema nodosum, even when there's no obvious kidney inflammation. With treatment, this problem may go away in a few months. In around 12 to 16 percent of individuals with leprosy, there are small traces of blood visible when examined under a microscope. This percentage is greater than the 0.5 to 2 percent observed in the general population.
Protein in the urine, called proteinuria, has been found in different studies, ranging from 2.1 percent to 68 percent. It is more common in the severe forms of leprosy with a higher number of bacteria. The amount of protein in the urine can be between 0.4 to 8.9 grams per day. A severe kidney condition called nephrotic syndrome is not common in leprosy, but there have been five cases reported in one type of leprosy (Virchowian form), with four cases occurring during a recreational state, and only two had abnormal deposits detected.
Leprosy's severe form is more commonly associated with reactional states and other unusual findings in the urine, such as specific structures (cylindruria) and white blood cells (leukocyturia). In the milder forms of leprosy, these unusual findings in the urine are not very common.
Glomerulonephritis -
It is the most frequent renal problem associated with leprosy. Research involving kidney biopsies revealed glomerulonephritis in more than 30 % of patients; this is greater than the 7 % found in studies examining kidneys after death (necropsy studies). The more severe form of leprosy has an even higher prevalence of glomerulonephritis.
What Histopathological Observations Are Evident in Leprosy Nephropathy?
Leprosy's wide range of histopathological lesions points to the disease's variable nature, even though its causes are not always distinct. Important histopathological findings of leprosy nephropathy include:
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Studies utilizing advanced techniques have identified the presence of immune complexes in renal tissues, characterized by deposits of IgG, C3 (occasionally IgA, IgM, and fibrin).
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Complement consumption in some cases strengthens the hypothesis that kidney issues in leprosy may be related to immune complex-mediated mechanisms.
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Various studies have provided additional insights into kidney abnormalities in leprosy. These include proliferative glomerulonephritis, membranous nephropathy, and mesangioproliferative glomerulonephritis.
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In some cases, rapidly progressive glomerulonephritis with acute kidney injury has been observed.
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Findings such as interstitial nephritis and amyloidosis were noted in certain individuals, contributing to the understanding of renal complications in leprosy.
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Chronic kidney disease linked to secondary amyloidosis has also been reported.
How Is Leprosy Nephropathy Treated?
Leprosy treatment involves specific therapy aimed at eliminating the causative bacterium, M. leprae. The goals include preventing immunological complications, avoiding physical deformities, and promoting both physical and psychosocial rehabilitation.
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WHO-Standardized Leprosy Therapy: The World Health Organization (WHO) recommends a standardized therapy for leprosy, which includes the use of Rifampicin, Dapsone, and Clofazimine.
Other considerations include:
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In cases of acute immunological episodes, Prednisone (1 to 2 mg/kg/day) and non-steroidal anti-inflammatory drugs (NSAIDs) may be given to control the inflammatory response.
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Erythema nodosum leprosum, which can have a prolonged course lasting months or years, is usually managed using NSAIDs, steroids, Thalidomide, Clofazimine, and Pentoxifylline. These drugs have the potential to cause kidney damage.
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In cases where leprosy leads to end-stage renal disease (ESRD), other options for treatment could include kidney transplantation or hemodialysis.
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Post-kidney transplant immunosuppression does not seem to alter the response of leprosy to drugs. However, there have been reports of acute, temporary deterioration in its course following transplantation.
Conclusion:
Renal involvement is a significant leprosy complication that needs to be looked into in each and every patient. The primary risk factor for kidney dysfunction in this disease appears to be multibacillary status. There have been reports of various glomerulopathies linked to leprosy. Specific treatment seems to impact on renal function improvement. To determine how leprosy nephropathy is progressing, regular monitoring of renal function via laboratory testing and imaging studies is crucial. Treatment modifications may be necessary depending on how the patient responds and how the renal complications develop.
