Katarzyna Jakuszko

Concurrent Infection of the Urinary Tract with Encephalitozoon cuniculi and Enterocytozoon bieneusi in a Renal Transplant Recipient

ABSTRACT A urinary tract coinfection, caused by Encephalitozoon cuniculi genotype II and Enterocytozoon bieneusi genotype D, was identified in an HIV-seronegative renal transplant recipient kept under lifelong immunosuppression. To our knowledge, this is the first report describing concurrent infection with these two microsporidia species in organ transplant recipients.

[Gender and kidney diseases: the clinical importance and mechanisms of modifying effects].

This review focuses on the underlying pathways of gender-dependent renal diseases and presents specific examples of diseases influenced by gender. In the literature it has been shown, in many clinical and experimental observations, that the incidence and the rate of progression of renal disease are influenced by many gender-dependent factors, such as kidney and glomerular size, differences in glomerular hemodynamics, and direct effects of sex hormones on renal tissue and signal pathways such as the renin-angiotensin-aldosterone system and signal molecules (e.g. nitric oxide, reactive oxygen species, cytokines and growth factors). It has been shown that the main female hormone, 17 β estradiol, is capable of inhibiting inflammatory and pro apoptotic processes and protects the renal tissue. In contrast, the male hormones, testosterone and dehydroepiandrosterone, have the opposite effect. Hormonal manipulation by male or female castration changes the course of renal disease progression and confirms the influence of the sex hormones. Female gender is therefore considered a protective factor in many kidney diseases, such as primary glomerulonephritis, autosomal dominant polycystic kidney disease (ADPKD) and hypertensive nephropathy. Similarly, women are more predisposed to autoimmune diseases with secondary glomerulonephritis, e.g. systemic lupus erythematosus, as the female sex hormones have the ability of autoimmune process activation. After menopause the protective effect of female gender is not observed, which confirms the role of the female sex hormones.

Prevalence and molecular characteristics of urinary and intestinal microsporidia infections in renal transplant recipients

Transplant recipients have been identified as a new risk group for microsporidia infection. We characterize for the first time the prevalence of microsporidia in intestinal and urinary tracts of renal transplant recipients. Molecular examination of 86 patients showed that 25.5% of them were infected; 86% were confirmed to have pathogens in their urine and 45.5% in stool. Among positive patients, 32% had microsporidia confirmed in both urine and stool. Genotyping revealed Encephalitozoon cuniculi (59%) and Enterocytozoon bieneusi (23%) monoinfections as well as coinfections with both species (18%). Moreover, we found diarrhoea and fever as symptoms significantly associated with microsporidia presence. Our results indicate that microsporidial infection should be considered in the assessment of renal transplant recipients, especially in the urinary tract, even if asymptomatic. Molecular identification of microsporidia species is relevant because of their different susceptibility for treatment.

Balloon Dilatation for Removal of an Irretrievable Permanent Hemodialysis Catheter: The Safest Approach.

Long-term hemodialysis catheter dwell time in the central vein predisposes to fibrin sheath development, which subsequently causes catheter malfunction or occlusion. In very rare cases, the catheter can be overgrown with fibrin and rigidly connected with the vein or heart structures. This makes its removal almost impossible and dangerous because of the possibility of serious complications, namely vein and heart wall perforation, bleeding, or catheter abruption in deep tissues. We describe two cases in which standard retrieval of long-term catheters was not possible. Balloon dilatation of catheter lumens was successfully used to increase the catheter diameter with simultaneous tearing of the fibrin sheath surrounding it. This allowed the catheter to be set free safely. Based on this experience, we present recent literature and our point of view.

Effective treatment of Kaposi sarcoma with everolimus in a patient with membranous glomerulonephritis.

A 78-year-old female patient with hypertension, atrial fibrillation, drug-induced diabetes mellitus and chronic kidney disease stage 3 was diagnosed with heavy nephrotic syndrome. A renal biopsy proved membranous nephropathy, serum antibodies against phospholipase A2 receptor (anti-PLA2R antibodies) were negative (Fig. 1A). The secondary causes of nephrotic syndrome were excluded. Tests for autoantibodies, viral infection (hepatitis B virus, hepatitis C virus, human immunodeficiency virus), serum protein electrophoresis and immunofixation for monoclonal protein were normal. Carcinoma antigens, except for Ca 125 antigen (132.3 U/mL, N: 0–35 U/mL), were negative. Transvaginal ultrasound revealed normal images of the uterus and ovaries and the presence of fluid in the Pouch of Douglas. We recognised that increased Ca 125 antigen corresponded to nephrotic syndrome. Due to persistent severe nephrotic syndrome with impaired renal function (serum albumin 17 g/L N: 35–52, total protein 42 g/L N: 66–83, daily proteinuria 7 g, serum creatinine 174 μmol/L, N: 62–115), the patient received steroids with the starting dose of 40 mg/day with cyclosporine of 125 mg/day (trough level 129.7 ng/mL), replaced after 2 months by tacrolimus 2 mg/day (trough 4.5 ng/mL). Partial remission of nephrotic syndrome was obtained (serum albumin 31 g/L, total protein 52 g/L, daily proteinuria 1.4 g). During the fifth month of the treatment, several lifted purple nodules appeared on the patient’s calves and shins. The lesions gradually spread to the thighs, the trunk and the left forearm (Fig. 1B). During the histopathologic examination of skin samples Kaposi sarcoma (KS) was identified (Fig. 1C,D). One month later, additional 5 mm maculopapular KS lesion developed in the right eye (Fig. 1E). The presence of serum anti-human herpesvirus-8 (HHV-8) IgG antibodies confirmed the history of infection.

Hepatitis C-associated glomerulonephritis mimicking systemic lupus erythematosus

Hepatitis C virus (HCV) infection is known to be responsible for many autoimmune reactions but its association with systemic lupus erythematosus (SLE) has not yet been established. We present the c...

Pathogenic role of antibodies against monomeric C‐reactive protein in tubulointerstitial nephritis and uveitis syndrome

Antibodies against monomeric C‐reactive protein, which is a target antigen expressed both in kidney tubules and uveal cells, have been recently detected in patients with active tubulointerstitial nephritis and uveitis syndrome. We report the case of an 65‐year‐old woman with acute renal failure caused by biopsy‐proven tubulointerstitial nephritis and the onset of uveitis 21 months later. The expression of monomeric C‐reactive protein in kidney oligobiopsy was confirmed by immunohistochemical staining using mouse monoclonal antibody against human monomeric C‐reactive protein. The levels of antibodies against monomeric C‐reactive protein were 117% of the reference during the flare and 22% during the remission of the disease. The difference in the levels of antibodies against monomeric C‐reactive protein during flare and remission, and above all positive biopsy staining, supports their pathogenic role in this disease.

[Pentraxins - their importance in pathogenesis of systemic lupus erythematosus].

Systemic lupus erythematosus (SLE) is an autoimmune disease, whose main pathomechanism is attributed to the disturbed apoptotic process and dysfunction of the immune cells, leading to the accumulation of undegraded cellular matrix. This paper presents molecules such as complement components, pentraxins, and collectins, which are involved in the opsonization and removal of cellular material, and shows how deficiencies in these processes may contribute to SLE development and progression. Many reports indicate the specific role of the pentraxins (C-reactive protein, serum amyloid P, pentraxin 3), which, due to enhancing the phagocytosis of damaged cells and inducing the classical pathway of complement activation, participate in masking antigens from the immune system. The influence of CRP on inhibition of development and progression of kidney disease and decreasing the immune activity markers was demonstrated on the basis of research in experimental, mouse models of SLE. The decreased pentraxin response described in systemic lupus erythematosus patients, despite the presence of high levels of interleukin-6 and other markers of disease activity, is still unclear. Anti-mCRP antibodies bind CRP to form immune complexes, which are deposited in glomeruli and may initiate or exacerbate inflammation. In the literature, the correlation between raised levels of anti-CRP antibodies and clinical and immunological activity of lupus nephritis was proved. It shows their importance as a factor determining the severity of the disease and response to treatment. Novel studies suggest that the low CRP response in SLE is due to interferon-α inhibition of gene expression and CRP synthesis. This suggests that therapeutic targets in systemic lupus erythematosus should also be based on inhibiting the synthesis of interferon-α .

How to Distinguish Patients with pSS among Individuals with Dryness without Invasive Diagnostic Studies

In the course of pSS, inflammatory cell infiltration consists mainly of lymphocytes infiltrating exocrine glands, which leads to their impaired function. The characteristic feature is generalized dryness. The aim of this study was to attempt to answer the question whether it is possible to distinguish between patients with pSS and individuals with dryness caused by other pathologies without applying invasive studies. The study included 68 patients with pSS and 43 healthy controls with dryness. FS ≥ 1 was observed in 90% of patients with pSS (with or without dryness), and only in 23% of the control group (only with xerostomia). In the pSS group, anaemia (p = 0.0085), lymphocytopenia (p = 0.0006), elevated ERS (p = 0.001), higher RF titer, and ANA antibodies were noted. Configuration of anti-SSA + SSB + Ro52 antibodies was characteristic for the pSS group. Considering the clinical symptoms, statistically significant differences were noted between pSS patients and the control group in frequency (p = 0.02) and severity (p = 0.042) of fatigue, lymphadenopathy, major salivary gland involvement, and photosensitivity to UV light. In conclusion, invasive methods are pivotal in pSS diagnosis in this salivary gland biopsy. Chronic fatigue syndrome is more common in pSS patients and can be subjective distinguishing factor in the group of people with dryness.

Antibodies against Pentraxins and Lupus Nephritis Activity

Impaired apoptosis and dysfunction of the immune cells are considered to be the most important pathogenic mechanisms of systemic lupus erythematosus. Pentraxins, which are natural opsonins, are directly involved in the removal of cellular material by binding to different antigens and initiating and enhancing phagocytosis of damaged cells. Therefore the deficiency of pentraxins is a crucial risk factor for the development and progression of systemic lupus erythematosus. Despite the presence of elevated levels of interleukin-6, which under physiological conditions increases the expression of acute phase protein genes, in systemic lupus a deficiency of C reactive protein and other pentraxins is observed. Several mechanisms responsible for pentraxin deficiency have been postulated, including the impairment of pentraxin synthesis due to mutations in genes, gene inhibition by interferon-α, and removal of pentraxins by autoantibodies. In this review, we summarize the significance of antibodies directed against pentraxins in assessing the activity and severity of systemic lupus erythematosus and lupus nephritis, as well as the usefulness of these antibodies as an additional marker of the response to treatment. The role of antibodies directed against monomeric C reactive protein in the pathogenesis of lupus nephritis is also discussed, as these antibodies are considered as a factor causing damage to the glomerular cells.