Kuddusi Cengiz

Increased Incidence of Tuberculosis in Patients Undergoing Hemodialysis

Tuberculosis was diagnosed in 26 patients (6 females and 20 males) undergoing maintenance hemodialysis, with an incidence of 23.6%. Infection was characterized clinically by a very insidious onset, the main symptoms being anorexia, loss of weight and low-grade fever, a very high sedimentation rate and lymphocytes predominant in the peripheral circulation, pleural and peritoneal fluids. Pulmonary tuberculosis was seen in 18 patients (70%), 10 of whom presented with pleural effusions. There were extrapulmonary presentations in 8 of the 26 patients (30%). Most of the patients developed the disease about 1 year from the start of their dialysis treatment. With early therapy all patients survived their tuberculosis disease and no recurrence was seen in up to 5 years of follow-up. Despite earlier reports of high mortality, we suggest that awareness of the increased incidence of tuberculosis in dialysis patients, together with its unusual presentation and consequent early diagnosis, results in a very good prognosis.

Increased incidence of neoplasia in chronic renal failure (20-year experience)

Patients with chronic renal failure (CRF) have a high incidence of malignant tumours. Uremia thus induces a remarkable suppression of immune status. In this study, we report that within the last 20 years, 188 (6.7%) various organ tumours were found in 2817 CRF patients that were hospitalised and treated. 69 (36.7%) of 188 patients with various organ tumours were on hemodialysis and the rest (63.3%) were CRF without hemodialysis. 49 (71%) of the 69 patients with hemodialysis were diagnosed with tumours in the first year of the hemodialysis therapy. In 110 (84%) of 119 CRF patients tumours were detected in less than 10 years after diagnosis of CRF. Localisation of the tumours were: 39 (19%) urologic malignancy, 30 (16%) parathyroid adenoma, 28 (15%) skin malignancy, 19 (10%) gynaecologic malignancy, 18 (9.5%) gastrointestinal tract (GIT) malignancy, 17 (9%) lung malignancy, 17 (9%) larynx malignancy, 13 (7%) thyroid malignancy, 5 (2.6%) multiple myeloma and 5 (2.6%) malignant lymphoma. No patients in the series had received a transplant kidney or were therapeutically immunosuppressed for other reasons and obstructive uropathy. CRF patients have a several times greater risk of developing malignant tumour than the general population.

Acute renal failure in leptospirosis in the black-sea region in Turkey

Leptospirosis is an infectious disease caused by pathogenic leptospires and is characterized by a broad spectrum of clinical manifestations, varying from inappearent infection to fulminant, fetal disease. Eighty-five to 90% of leptospirosis infections are self-limiting. However, 5–10% of infection by L.interrogans can cause renal tubular damage, microvascular injury, acute renal failure (ARF), and interstitial nephritis.We studied 36 patients with leptospirosis. Twenty-seven (65%) cases of 36 patients had ARF. Fourteen (51%) had nonoliguric ARF. In thirteen (48%) oliguria appeared on the third or fourth days of hospitalization. Serum BUN, creatinine, serum bilirubine, ALT, AST, potassium and thrombocytopenia levels were higher in oliguric than nonoliguric patients (p < 0.05). However, serum sodium, CPK levels were not different between oliguric and nonoliguric groups (p > 0.05). Thirteen patients (48%) needed in renal replacement therapy (RRT). 8 of them were treated by hemodialysis (HD) alone and 5 patients by HD in combination with hemoperfusion. Twenty-five patients (92%) recovered completely after 3–5 weeks. Two patients (7.4%) who had severe hepatorenal and hemorrhagic syndromes, died.We concluded that till now leptospirosis is actual problem for nephrologist in the developing countries because of very high percentage of renal disease, with good prognosis in patients without multiorgan failure and early treatment.

Periodontal disease in patients with familial Mediterranean fever: from inflammation to amyloidosis

BACKGROUND AND OBJECTIVE Familial Mediterranean fever stimulates a very intense acute-phase reactants response and if left untreated eventually leads to amyloidosis. The aim of this study was to determine the prevalence of periodontal disease among patients with familial Mediterranean fever in the Black Sea region in Turkey and to evaluate whether periodontitis is related to amyloidosis in patients with familial Mediterranean fever. MATERIAL AND METHODS One-hundred and thirty three patients with familial Mediterranean fever and 50 healthy subjects were included in this study. Periodontal health and disease were evaluated using the gingival index, papillary bleeding index, plaque index and periodontal disease index. The concentrations of serum acute-phase reactants were measured at baseline and at 4-6 wk after completion of the nonsurgical periodontal therapy. Genetic testing for familial Mediterranean fever was performed using the familial Mediterranean fever StripAssay. Kidney biopsy was carried out on all proteinuric patients. RESULTS The prevalence of moderate to severe periodontitis in familial Mediterranean fever patients with amyloidosis (80.6%) was significantly greater (p < 0.01) than in familial Mediterranean fever patients without amyloidosis (38%) and in controls (20%). Serum levels of acute-phase reactants in familial Mediterranean fever patients were reduced significantly following nonsurgical periodontal therapy (p < 0.01). CONCLUSION Periodontal therapy seems to reduce the serum levels of acute-phase reactants in patients with familial Mediterranean fever. Therefore, treating periodontitis might help to alleviate the disease burden in patients with familial Mediterranean fever.

Should Tuberculosis Prophylaxis Be Given for the Chronically Dialyzed Patients

Accessible online at: www.karger.com/journals/nef Until the middle of this century, tuberculosis was, in Dickens’ words, ‘a disease which medicine never cured, wealth warded off, or poverty could boast exemption from – which sometimes moves in giant strides, and sometimes at a tardy sluggish pace, but, slow or quick, is ever sure and certain’ [1]. Mycobacterium tuberculosis is an extremely successful pathogen that continues to thrive in developing countries and is re-emerging in the industrialized world. Globally, it remains a more frequent cause of death than any other infectious agent [2]. Approximately a third of the world’s population is infected with M. tuberculosis, and the World Health Organization estimated that in 1996 there were 8 million new cases of tuberculosis and 3 million deaths from the disease [2]. The sinister synergy between this disease of antiquity and the newer pathogen human immunodeficiency virus is responsible for the death of about a third of all patients with AIDS in Africa [3]. Yet progression to disease and death is far from an inevitable consequence of exposure. There is dramatic variability in the rates of infection among persons exposed to different sources of infection, and of those infected, approximately 90% never become ill. The inability to predict whose patients are most likely to transmit infection and who among those infected will have the disease and infect others remains a major barrier to optimal public health and patient care. Host resistance to M. tuberculosis is mediated by cellular immunity as this is impaired in patients with chronic renal failure [4], the incidence of tuberculosis in dialyzed patients should be high. Cellular and humoral immune responses are suppressed in uremic subjects [5]. The increase in sister chromatid exchange (SCE), chromosal aberrations, tumor markers and the impaired cell function have been reported [6–8]. Uremia thus induces a remarkable suppression of the immune status. In addition, patients receiving hemodialysis spend prolonged periods of time together in health-care facilities, thereby increasing the potential for tuberculosis transmission if a patient has active disease. For these reasons, routine tuberculosis screening of hemodialysis patients has been recommended [9]. Although the Mantoux tuberculin skin test remains the most useful screening tool, cutaneous anergy decreases the accuracy of the test. End-stage renal failure patients on chronic dialysis are prone to tuberculous infection due to a defect in cellular immunity. The incidence is reported to be 10–16 times higher than that in the general population [10–14]. One in every 3 people in the world is infected with M. tuberculosis, and observed rates of new tuberculosis infection are on the increase, especially in the third world [15–18]. In the ‘rich’ countries, latent tuberculosis can be reactivated in a number of ‘high-risk’ patient populations such as AIDS, silicosis, immunosuppression, malnutrition and end-stage renal failure [15–17]. Worldwide tuberculosis

Hypothyroidism as a Cause of Resistance to Erythropoietin

Accessible online at: www.karger.com/journals/nef Dear Sir, A poor response to human recombinant erythropoietin (EPO) is seen in 5–10% of the patients with renal anemia. Several factors, such as iron deficiency, blood loss, infections, inflammatory conditions, hyperparathyroidism, aluminum toxicity, vitamin B12 or folate deficiency, red cell enzyme defects, hemoglobinopathies, and hemolysis, have been shown to inhibit a response to EPO [1]. Hypothyroidism may lead to anemia. The aim of this report is to present a hypothyroid hemodialysis patient with a diminished response to EPO. A 50-year-old female patient was admitted to the University Hospital because of a poor response to EPO. She had autosomal dominant polycystic kidney disease, hypertension, and a history of thyroidectomy. She was treated with regular hemodialysis (three times weekly during the last year, twice weekly before) for 5 years. Her hemoglobin and hematocrit values were 6.7 g/dl and 20%, respectively, after 1 year of EPO treatment (4,000 U s.c. three times weekly). Iron (parenteral and oral supplementation), folate, amlodipine, vitamin D, phosphorus binders, and levothyroxine (100 Ìg/day) were the other medications of the patient. In order to define the underlying mechanism of the EPO resistance, she underwent a hematological survey which yielded the following results: serum iron 39 Ìmol/l, serum iron binding capacity 160 Ìmol/l, serum ferritin 611 ng/ml, serum vitamin B12 240 pg/ml, and serum folate 6 ng/ml. A peripheral blood smear showed normochromic, normocytic erthyrocytes with normal leukocytes and platelets. A bone marrow aspiration biopsy revealed a normocellular marrow. There were no clinical or laboratory findings suggesting blood loss, infection, or inflammation. Thyroid function tests revealed free triiodothyronine 1.01 pmol/l, free thyroxine 0.74 pmol/l, and thyroid-stimulating hormone 48 mIU/l. The dosage of levothyroxine was increased to 150 Ìg/day, later to 200 Ìg/ day. Three months thereafter, her hemoglobin and hematocrit values rose to 11.8 g/dl and 37%, respectively, with suppression of thyroid-stimulating hormone. Three years later, the patient is now receiving EPO at a dosage of 4,000 U three times weekly, and her hemoglobin and hematocrit values are within the desired limits. These findings support that underlying hypothyroidism is the cause of resistance to EPO treatment in this patient. The requirement of an euthyroid state for the action of EPO on the bone marrow is well known, but only 1 hypothyroid hemodialysis patient with a poor response to EPO has been reported previously [2]. Hypothyroidism should be included in the differential diagnosis of a poor response to EPO in patients with renal failure.

Interaction Between Periodontal Disease and Systemic Secondary Amyloidosis: From Inflammation to Amyloidosis

BACKGROUND It has become increasingly clear in recent years that periodontal disease can cause a dramatic increase in the levels of markers of systemic inflammation, and that periodontal treatment can result in reduction in the levels of these markers. We have previously shown that the prevalence of moderate to severe periodontitis was significantly higher in patients with familial Mediterranean fever (FMF) with amyloidosis than in patients with FMF without amyloidosis. Thus, the aim of this study is to investigate if chronic periodontitis is associated with secondary amyloidosis in the Black Sea region of Turkey. METHODS A total of 112 patients with biopsy-proven secondary amyloidosis (59 patients with FMF, 40 patients who were either chronically infected or had malignant disease, 13 patients with periodontitis) and 22 healthy subjects, were included in this study. Periodontal health and disease were evaluated using gingival index (GI), papillary bleeding index (PBI), plaque index (PI), and periodontal disease index (PDI). The concentrations of serum acute phase reactants (APRs) were measured at baseline and at 4 to 6 weeks after completion of the non-surgical periodontal therapy. RESULTS The prevalence of moderate to severe periodontitis was 47.5% in patients with FMF, 72.5% in patients who were either chronically infected or had malignant disease, and 84.6% in patients with periodontitis. Serum levels of APRs in patients with amyloidosis were reduced significantly after non-surgical periodontal therapy (P <0.01). CONCLUSIONS Periodontitis can increase the levels of APRs and potentiate the development of amyloidosis either by themselves or association with traditional factors, such as FMF and other chronic inflammatory diseases. Thus, preventing or treating periodontitis might prevent or at least alleviate the progression of amyloidosis. Periodontal evaluation should be performed as part of a medical assessment and considered as an etiologic factor for secondary amyloidosis.

CT and ultrasound of abdominal hemorrhage in Henoch-Schönlein purpura

Abstract We report the CT and ultrasound findings of renal, gallbladder, and liver hemorrhage in a 24-year-old patient with Henoch-Schonlein purpura.

Red Cell Distribution Width and Mean Platelet Volume in Amyloidosis

We aimed to determine whether red cell distribution width (RDW) and mean platelet volume (MPV) values differ between patients with reactive amyloid A (AA) amyloidosis due to chronic inflammatory disease and in healthy participants. In this study, 33 patients with AA amyloidosis and 40 age- and sex-matched healthy controls were enrolled. Erythrocyte sedimentation rate (ESR), RDW, platelet count (PLT), and MPV levels were retrospectively obtained from our computerized patient database. We found RDW, ESR, and PLT levels to be significantly higher in patients with AA amyloidosis compared with the controls (P < .0001). Mean platelet volume was significantly lower in patients with amyloidosis (P < .0001). Inflammatory diseases such as AA amyloidosis may demonstrate low MPV and high RDW levels.

Lipoprotein abnormalities in patients with secondary renal amyloidosis

The prevalance of hyperlipidemia in chronic renal failure (CRF) patients is higher than in general population. Secondary amyloidosis is a common cause of CRF in Turkey. In this study, 25 patients with CRF due to secondary renal amyloidosis (amyloid-CRF), 15 patients with CRF without amyloidosis-CRF and 17 healthy controls were studied for serum lipid parameters. The mean serum lipoprotein (a) [LP(a)] level in the patients with amyloid-CRF was significantly higher than in the controls (p < 0.01). The mean serum apolipoprotein B (Apo B), apolipoprotein E (Apo E) and triglyceride levels in the patients with amyloid-CRF were very significantly higher than in the controls (p < 0.001). The mean serum total cholesterol, low- density lipoprotein (LDL) levels in the patients with amyloid-CRF were higher than in the controls (p < 0.05). The mean serum apo AI levels in the patients with amyloid-CRF was very significantly lower than in the controls (p < 0.001).The mean serum high-density lipoprotein (HDL) in the patients with amyloid-CRF was lower than in the controls (p < 0.05). The mean serum Lp (a), Apo AI, Apo B and Apo E levels in the patients with amyloid-CRF were significantly higher than in the patients with CRF (p < 0.01). The mean serum total cholesterol, trigliserides, LDL and HDL levels in the patients with amyloid-CRF were higher than in the patients with CRF (p < 0.05).There was not any correlation with serum lipid parameters and serum albumin and urine protein levels (p < 0.05).Our study suggests that serum lipid parameters are abnormal and might be the risk factor of atherosclerotic vascular disease and contribute to renal disease progression in the patients with secondary renal amyloidosis and lipid abnormalities were different from CRF with various etiology, without amyloidosis.