Excessive Protein Loss Research Articles

Regulation of cholesterol homeostasis in osteoporosis mechanisms and therapeutics.

Osteoporosis is a metabolic bone disease that affects hundreds of millions of people worldwide and is characterized by excessive loss of bone protein and mineral content. The incidence and mortality of osteoporosis increase with age, creating a significant medical and economic burden globally. The importance of cholesterol levels has been reported in the development of diseases including osteoporosis. It is important to note that key enzymes and molecules involved in cholesterol homeostasis are closely related to bone formation. Excessive cholesterol may cause osteoporosis, cholesterol and its metabolites affect bone homeostasis by regulating the proliferation and stimulation of osteoblasts and osteoclasts. Therefore, antagonism of elevated cholesterol levels may be a potential strategy to prevent osteoporosis. There is sufficient evidence to support the use of bisphosphonates and statin drugs for osteoporosis in the clinic. Therefore, in view of the aggravation of the aging problem, we summarize the intracellular mechanism of cholesterol homeostasis and its relationship with osteoporosis (including cholesterol and cholesterol oxidation products (COPs) in osteoporosis). Furthermore, the current clinical cholesterol-lowering drugs for osteoporosis were also summarized, as are new and promising therapies (cell-based therapies (e.g., stem cells) and biomaterial-delivered target drug therapies for osteoporosis as well).

Allergy to Cow’s Milk Proteins and Other Allergens—An Unrecognized Co-Factor of Idiopathic Nephrotic Syndrome in Children or a Factor Interfering with the Treatment of This Disease? A Case Report

Idiopathic nephrotic syndrome (INS) is one of the chronic kidney diseases that occurs in childhood. Starting from a few case reports in the 1950s–1970s and up to the present, the relationship between idiopathic nephrotic syndrome (INS) and the occurrence of atopic disorders in these patients has been discussed in many medical publications. These publications show that in certain patients, mainly children and adolescents, but also in adults with INS, various clinical symptoms and laboratory indicators of an atopic allergic process may be present. This process has been shown to involve Th2 lymphocytes, to have an excessive production of interleukins (IL-4, IL-5, IL-13), and to have an increased serum level of immunoglobulin E (IgE). This leads to the development of a systemic allergic inflammatory process, of which the kidneys can also become the effector organ. The coexistence of an allergic process which may adversely affect the course of nephrotic syndrome may be confirmed by the increased serum IgE level and the hypersensitivity reaction of the patient’s body to various environmental allergens (through the presence of allergen-specific IgE /asIgE/ antibodies to food, pollen, mould, dust, or other allergens in the blood serum). High concentrations of IL-13 and other plasma mediators of this inflammation (e.g., histamine, bradykinin) structurally and functionally damage the renal filtration barrier, and in particular, the function of podocytes in the glomeruli. Podocyte dysfunction disturbs the physiological process of plasma filtration in the glomeruli, leading to excessive protein loss in the urine. These disorders initiate the development of idiopathic nephrotic syndrome in these patients. This publication presents the coexistence of an allergic process caused by allergy to cow’s milk proteins and hypersensitivity to other allergens in a child with idiopathic nephrotic syndrome. This publication also assesses whether treatment of the allergic process coexisting with INS with an elimination diet (milk-free, hypoallergenic) and anti-allergic drugs affected the course and treatment of INS in this child.

The long-term clinical course of protein-losing enteropathy combined with iron deficiency anemia in Korean toddlers: Possible association with cow's milk protein.

Protein-losing enteropathy (PLE), a rare condition with excessive gastrointestinal protein loss, presents with hypoalbuminemia, edema, or ascites. Several cases of PLE combined with severe iron deficiency anemia (IDA) have been reported in infants and toddlers that were considered to result from excessive cow's milk consumption, although the mechanism has not been clearly established. We retrospectively reviewed the clinical, laboratory, endoscopic, and radiologic characteristics of patients diagnosed and treated for PLE with IDA between 2015 and 2021. Long-term outcomes were analyzed according to dietary intervention during the follow-up period. A total of 10 patients aged 7.0-26.7 months were enrolled in the study and the median follow-up duration of them was 9.4 months (range, 1.3-18.0). Six of them were fed powdered formula, while two were fed whole cow's milk, and their median daily intake was 700mL (range, 300-900). The times to normalization of hemoglobin, albumin, and eosinophil count were shorter in patients with dietary elimination of cow's milk protein immediately after diagnosis compared to those with reduced intake or no dietary change. Early complete elimination of cow's milk protein should be considered, especially if the laboratory parameters are not normalized with adequate iron supplementation even though the clinical symptoms show improvement. We would like to draw attention to the possibility of the cow's milk protein in the pathogenesis of the condition through the non-IgE-mediated immune reactions.

Kwashiorkor is a Six-year-old, Presenting as Acrodermatitis Enteropathica

Background: Protein-energy malnutrition (PEM) is commonly seen in developing countries, especially in infants and young children up to 5 years of age. Edema is one of the characteristic features which occurs due to excessive protein loss or decreased protein intake. It is one of the rising concerns of parents and leads to mortality if untreated.
 Case Presentation: A 6-year-old male child was brought with complaints of excessive skin lesions and loss of appetite for four months. He sustained burns on his legs four months back, and his general condition worsened at home. Protein-energy malnutrition (PEM) is common among children 6-59 months. The age of presentation in our patients is unusual. We stepped up his nutritive intake, added micronutrients and trace elements, and he recovered with our efforts.
 Conclusion: We recognized the child’s underlying condition well and started the apt treatment. The child responded well to the nutritional intervention and showed signs of recovery. The age of presentation was rare, which has made us report the case. The parents were counseled well to step up the child’s protein and calorie intake and ensure a tender and stress-free environment at home, enhancing the child’s recovery.

A STUDY ON SERUM IRON, TRANSFERRIN AND FERRITIN LEVELS IN NEPHROTIC SYNDROME PATIENTS AT HUE UNIVERSITY OF MEDICINE AND PHARMACY HOSPITAL

Background: The prolonged and excessive loss of protein through urine in nephrotic syndrome patients decreases blood protein and leads to other changes such as dyslipidemia, disorders of blood components, hematopoiesis…., if the blood albumin level decreases continuously, the more obvious these disorders, the serum iron, transferrin and ferritin levels will be changing. The aim of the study was to determine the concentrations of serum iron, transferrin, ferritin in nephrotic syndrome patients and the relation between these parameters. Materials and methods: Descriptive cross-sectional studies of 68 patients with the diagnosis of nephrotic syndrome and without renal failure. Results: The mean concentration of serum iron was 8.9 μmol/L, with the low level was 30.9%. While the serum transferrin which was lower than normal was 100% and the mean concentration was 0.68 mmol/L. The mean concentration of serum ferritin was 610.3 pmol/L, and its high level was 67.6%. Conclusions: Concentration of serum ferritin was elevated and inversely correlated with serum iron and transferrin concentrations. Key words: iron, transferrin, ferritin, nephrotic syndrome

Study on Changes of the Concentration of Some Indicators of the Serum Iron Test in Patients with Nephrotic Syndromein Vietnam

Background: In nephrotic syndrome (NS), the excessive and prolonged loss of protein in the urine reducesalbumin blood and leads to many other changes such as dyslipidemia, blood clotting disorders, and disordersof hematopoietic components. In NS, the more persistent and persistent decrease in albumin in the blood, themore apparent these disorders, including disorders of iron, transferrin and ferritin in serum. The objectivesof the study were to: Determine serum iron, transferrin and ferritin concentrations and Investigate therelationship between iron, transferrin and ferritin concentrations and serum albumin in NS patients.Methodology: Cross-sectional descriptive research method. Convenient and controlled sample selectionof 68 NS patients without kidney failure, aged 16 years and over, hospitalized for treatment at InternalDepartment of Hue University of Medicine and Pharmacy Hospital, Vietnam.Results: The average serum iron concentration is 8.9 µmol/L, of which at low level, the rate is 30.9%; In100% of cases, the serum transferrin concentration is lower than normal, the average concentration is 0.68mmol/L; the average elevation of ferritin in serum was 610.3 pmol/L, of which at high level accounted for67.6% (46 patients). Serum albumin concentrations are positively correlated with iron and transferrin, butnegatively with serum ferritin.Conclusion: In NS, the serum ferritin concentration is elevated and inversely correlated with the serum iron,transferrin, and albumin concentration.

Validity of Three-Dimensional Tortuous Pore Structure and Fouling of Hemoconcentration Capillary Membrane Using the Tortuous Pore Diffusion Model and Scanning Probe Microscopy.

Hemoconcentration membranes used in cardiopulmonary bypass require a pore structure design with high pure water permeability, which does not allow excessive protein adsorption and useful protein loss. However, studies on hemoconcentration membranes have not been conducted yet. The purpose of this study was to analyze three-dimensional pore structures and protein fouling before and after blood contact with capillary membranes using the tortuous pore diffusion model and a scanning probe microscope system. We examined two commercially available capillary membranes of similar polymer composition that are successfully used in hemoconcentration clinically. Assuming the conditions of actual use in cardiopulmonary bypass, bovine blood was perfused inside the lumens of these membranes. Pure water permeability before and after bovine blood perfusion was measured using dead-end filtration. The scanning probe microscopy system was used for analysis. High-resolution three-dimensional pore structures on the inner surface of the membranes were observed before blood contact. On the other hand, many pore structures after blood contact could not be observed due to protein fouling. The pore diameters calculated by the tortuous pore diffusion model and scanning probe microscopy were mostly similar and could be validated reciprocally. Achievable pure water permeabilities showed no difference, despite protein fouling on the pore inlets (membrane surface). In addition, low values of albumin sieving coefficient are attributable to protein fouling that occurs on the membrane surface. Therefore, it is essential to design the membrane structure that provides the appropriate control of fouling. The characteristics of the hemoconcentration membranes examined in this study are suitable for clinical use.

Artesunate inhibits osteoclastogenesis through the miR-503/RANK axis.

Osteoporosis is a metabolic bone disease that is characterized by decreased bone density and strength due to excessive loss of bone protein and mineral content, which can be induced by increased osteoclast activity. Developing agents targeting osteoclast activation is considered to be the most effective method to reverse bone destruction and alleviate the pain caused by osteoporosis. MTT assay was conducted to detect the cell viability after artesunate treatment of RAW264.7 cells. TRACP staining and pit formation assays were performed to examine the TRACP-positive cells and pit-forming activity of osteoclasts. qRT-PCR and Western blot analysis were performed to assess the mRNA and protein expression levels of the osteoclastogenesis-related genes NFATc1, TRAP, and cathepsin k. The protein levels of RANK, p-Akt, p-p38, and p-ERK were examined by Western blotting. Luciferase reporter assay was conducted to determine whether miR-503 targeted RANK directly. Artesunate inhibited TRACP-positive cells and the pit-forming activity of osteoclasts. However, artesunate increased the expression of miR-503. Artesunate suppressed osteoclastogenesis-related gene expression and RANKL-induced activation of MAPKs and the AKT pathway. In addition, miR-503 inhibited RANK expression by directly targeting RANK during osteoclast differentiation. Artesunate inhibited osteoclastogenesis and osteoclast functions in vitro by regulating the miR-503/RANK axis and suppressing the MAPK and AKT pathways, which resulted in decreased expression of osteoclastogenesis-related markers.

Nefrotik Sendrom ve Tıbbi Beslenme Tedavisi

Vücuttan aşırı protein kaybı ile karakterize bir durum olan nefrotik sendrom organizmada pek çok defekte neden olabilmektedir. Nefrotik sendromun tedavi edilememesi ile birlikte de geri dönüşümsüz böbrek yetmezliğine neden olarak, ilerleyen dönemde bireyin hayatını tehlikeye sokacak sağlık sorunlarının yaşanmasına yol açabilmektedir. Proteinüri, ödem ve köpüklü idrar nefrotik sendromun sıklıkla görülen belirtileri arasındadır. Nefrotik sendromun tedavisi tıbbi beslenme tedavisi, tıbbi tedavi, immün sistem baskılayıcı tıbbi tedavi kullanılarak yapılabilmektedir. Nefrotik sendromlu hastalarda progresif böbrek yetmezliğinin önlenebilmesi için tıbbi beslenme tedavisinin önemi büyüktür. Nefrotik sendromlu hastalarda azot dengesinin korunabilmesi için yeterli enerji vermek önemlidir. Yine kas kaybının ve malnütrisyonun önlenebilmesi, proteinürinin dengelenebilmesi açısından da yeterli protein sağlanmalıdır. Nefrotik sendromda görülen komplikasyonlarından birisinin de hiperlipidemi olması nedeni ile diyet yağının tür ve miktarının da önemli olduğu vurgulanmaktadır. Sonuç olarak, tedavi edilemediği takdirde böbrek yetmezliğine neden olabilecek nefrotik sendromun kontrol altında tutulmasında tıbbi beslenme tedavisinin öneminin büyük olduğu düşünülmektedir. Bu derleme ile de nefrotik sendromda tıbbi beslenme tedavisinin açıklanması amaçlanmıştır.

Ascites Index - an attempt to objectify the assessment of ascites.

Introduction: Ascites is observed in cancer patients as well as in other non-neoplastic processes. In some patients, it may cause severe symptoms that can become directly life-threatening. The assessment of the degree of ascites seems useful in the determination of treatment effects as well as in the monitoring of fluid accumulation and early planning of decompression procedures. Aim: Determination of the clinical usefulness of a quantitative method of determining the degree of ascites, so-called Ascites Index. Material and methods: The Ascites Index is an ultrasonographic way of assessing the grade of ascites. The examination result is an index which is analogous to the amniotic fluid index determined in pregnant patients. The Ascites Index was determined in patients with ascites in the course of stage III–IV ovarian carcinoma (7 patients) and ovarian hyperstimulation syndrome (12 patients). Results: The patients with ovarian hyperstimulation syndrome required decompressive paracentesis at the median Ascites Index above 290 mm (range: 216–386 mm). In the patients with ovarian carcinoma, the median value of the Ascites Index at which paracentesis was required was 310 mm (range: 273–389 mm). To avoid complications associated with excessive protein loss, 2000 mL of fluid was evacuated at a single occasion. Following the procedure, the median value of the Ascites Index was 129 mm (range: 121–145 mm) in the patients with ovarian hyperstimulation syndrome and 146 cm (119–220 mm) in cancer patients. Conclusions: The proposed index is simple and rapid to determine. It makes evaluation of the degree of ascites considerably easier. Moreover, it only minimally burdens patients and enables assessment of the effect of decompression or treatment. It seems that this method might be useful also in the assessment of ascites caused by other factors, but this requires further clinical studies.

Application of automated peritoneal dialysis in urgent-start peritoneal dialysis patients during the break-in period

ObjectiveWhether automated peritoneal dialysis (APD) is a feasible strategy for urgent-start peritoneal dialysis (PD) therapy during the break-in period remains unclear. This study was conducted to compare the efficacy as well as complications among three PD modes during the break-in period.MethodsNinety-six patients treated with urgent-start PD after catheterization were retrospectively analyzed. Patients were divided into three groups, incremental continuous ambulatory PD (CAPD) group (n = 26); APD group (n = 42); and APD–CAPD group (n = 28). Clinical parameters at the end of the break-in period and 1 month after the initiation of PD treatment were collected and analyzed.ResultsCompared with the traditional incremental CAPD, APD and APD–CAPD were superior as they could effectively remove small-molecule uremic toxins and correct electrolyte imbalance (P < 0.05), while did not increase the incidence of early complications during the break-in period (P > 0.05). However, APD led to a significant decline in albumin and pre-albumin, as compared with APD–CAPD and CAPD (P < 0.05). A PD strategy consisting 6 days of APD and 3 days of CAPD showed a great advantage in preventing excessive protein loss. There were no significant differences in all tested biochemical parameters among the three groups at 1 month after treatment (all P > 0.05).ConclusionApplication of APD for urgent-start PD during the break-in period is feasible. A combination of APD and CAPD regimens seems to be a more reasonable mode.

Protein-Losing Hypertrophic Gastropathy, Menetrierʼs Disease, Successfully Managed With Long-Acting Octreotide

Protein-losing gastro-enteropathies are characterized by excessive loss of protein into the gastrointestinal tract. Ménétrier's disease (MD) is a rare disease characterized by extreme foveolar hyperplasia with glandular atrophy in a patient with gross enlargement of gastric folds or ruggae. Little is understood about the pathogenesis of this disease and treatment has mostly consisted of dietary therapy (low-fat, high-protein, medium-chain triglyceride diet.) This case describes a patient with MD successfully managed with Octreotide until he developed intussusception of a large gastric adenoma which required an emergent gastrectomy. A 52 yo AA male was diagnosed with MD after evaluation of a large gastric mass/thickened fold incidentally noted on imaging. An EGD confirmed thickened and large gastric folds. Gastric biopsies demonstrated dilated hyperplastic foveolar glands with stromal edema making the diagnosis of MD (Figure 1, 2). His course was complicated by several hospitalizations for DVTs treated with anticoagulation, severe intra-abdominal hemorrhage due to a complicated LVP, complicated pancreatic fluid collections, volume over load, and severe symptomatic anemia. Labs revealed a hemoglobin of 2.6 g/dL (MCV 58), ferritin 8 ng/ml, iron of < 5 mcg/dL, and Albumin of 0.9 g/dL. For several weeks his Albumin persistently ranged between 0.9 - 1.3 g/dL. Further evaluation revealed an elevated alpha-1-antitrypsin stool clearance >59 ml/day. He was started on octreotide 100mg BID SQ x6 months and subsequently transitioned to long acting Octreotide 20mg IM q4weeks. His albumin increased from 0.9 g/dL to 2.9 g/dL over the following 12-months. His anemia, microcytosis, and iron deficiency normalized. All of his clinical manifestations of hypoalbuminemia resolved and he regained significant muscle mass. Unfortunately, almost 19-months after making the diagnosis of MD he developed a gastric outlet obstruction due to a large fungating gastric adenoma filling and markedly distending the duodenum necessitating an emergent gastrectomy. He recovered well from surgery and continues to do well upon on follow up. Our case demonstrates the potential role of Octreotide as treatment or bridge to surgery for management of patients with protein losing gastropathies as well as as a gastric outlet obstruction from a gastric adenoma, an uncommon complication of this rare disease.Figure: Endoscopic appearance of the stomach showing mucosa edema and polypoid changes of the gastric fundus and body.Figure: Gastrectomy is performed. A, Grossly, there is hypertrophy of the fundal and body mucosa with sparing of the gastric antral mucosa; B-D, histologically, the body and fundal mucosa shows edematous, mildly inflamed lamina propria with hyperplastic.

Matrine prevents bone loss in ovariectomized mice by inhibiting RANKL-induced osteoclastogenesis.

Osteoporosis is a metabolic bone disease characterized by decreased bone density and strength due to excessive loss of bone protein and mineral content. The imbalance between osteogenesis by osteoblasts and osteoclastogenesis by osteoclasts contributes to the pathogenesis of postmenopausal osteoporosis. Estrogen withdrawal leads to increased levels of proinflammatory cytokines. Overactivated osteoclasts by inflammation play a vital role in the imbalance. Matrine is an alkaloid found in plants from the Sophora genus with various pharmacological effects, including anti-inflammatory activity. Here we demonstrate that matrine significantly prevented ovariectomy-induced bone loss and inhibited osteoclastogenesis in vivo with decreased serum levels of TRAcp5b, TNF-α, and IL-6. In vitro matrine significantly inhibited osteoclast differentiation induced by receptor activator for NF-κB ligand (RANKL) and M-CSF in bone marrow monocytes and RAW264.7 cells as demonstrated by tartrate-resistant acid phosphatase (TRAP) staining and actin-ring formation as well as bone resorption through pit formation assays. For molecular mechanisms, matrine abrogated RANKL-induced activation of NF-κB, AKT, and MAPK pathways and suppressed osteoclastogenesis-related marker expression, including matrix metalloproteinase 9, NFATc1, TRAP, C-Src, and cathepsin K. Our study demonstrates that matrine inhibits osteoclastogenesis through modulation of multiple pathways and that matrine is a promising agent in the treatment of osteoclast-related diseases such as osteoporosis.—Chen, X., Zhi, X., Pan, P., Cui, J., Cao, L., Weng, W., Zhou, Q., Wang, L., Zhai, X. Zhao, Q., Hu, H., Huang, B., Su, J. Matrine prevents bone loss in ovariectomized mice by inhibiting RANKL-induced osteoclastogenesis.

Changes in the metabolic profile and body weight of pre-pubertal gilts during prolonged monotonic exposure to low doses of zearalenone and deoxynivalenol

The aim of this study was to determine whether exposure to low doses of ZEN + DON induces changes in serum biochemical and hematological parameters in pre-pubertal gilts. In the evaluated groups, minor but statistically significant changes were noted in selected serum biochemical parameters, including glucose, total cholesterol, ALT, AST, AP, total bilirubin, Pin, Fe, K and Cl, and in hematological parameters, including WBC, eosinophils, basophils, monocytes, Ht, Hb, MCHC, HDW and PLT. A statistical analysis of the results revealed significant differences between groups in the values of WBC, eosinophils, basophils, Hb, Ht, PLT, glucose, ALT, AP, total bilirubin, Fe and K. Change trends were noted mainly in weeks II and V-VI. An analysis of the metabolic profile of pre-pubertal gilts exposed to ZEN + DON indicates that homeostasis and biotransformation of ZEN + DON can be toned down at the expense of the animals' energy reserves. Body weight gains were lower in group E, and BW gains were not observed in weeks II and VI. The activity levels of gilts decreased in the first weeks of exposure (I and II), but the drop was minimized by a compensatory effect, or in the last two weeks of exposure due to nutrient deficiency or insufficient supply of protein and energy with feed and feed additives, which decreased BW gains. Low doses of mycotoxins induce completely different changes in the metabolic test than higher doses. The above can probably be attributed to: (i) a negative compensatory effect, (ii) initiation of adaptive mechanisms and stimulation of the immune system, probably due to the allergizing properties of mycotoxins, (iii) excessive loss of energy and protein due to more effective feed utilization, or (iv) involvement in detoxification processes which leads to fatigue. Depending on the body's energy stores, the above processes tend to tone down the biotransformation of low doses of the examined mycotoxins but in the present study, the BW of gilts did not increase under exposure to a combination of ZEN + DON.

Diagnostic delay in clinical practice: A case report of Coeliac disease

Once considered a gastrointestinal disease of childhood affecting mainly whites, Coeliac Disease is now recognized as a systemic disease that may affect persons of any age and many races and ethnic groups. In this paper we present a case of a 60-year-old woman presented with protein-losing enteropathy associated with partial villous atrophy on distal duodenal biopsy. In Coeliac enteropathy the changes in intestinal permeability is sufficient to cause excessive loss of protein into the gut leading to hypoproteinaemia. The patient had presented with peripheral oedema without liver or renal impairment. The case emphasizes that clinicians should have a heightened suspicion about the disease that may be present at any age in both sexes and in a wide variety of clinical circumstances.

Marginal Zone Lymphoma Complicated by Protein Losing Enteropathy.

Protein losing enteropathy (PLE) refers to excessive intestinal protein loss, resulting in hypoalbuminemia. Underlying pathologies include conditions leading to either reduced intestinal barrier or lymphatic congestion. We describe the case of a patient with long-lasting diffuse abdominal problems and PLE. Repetitive endoscopies were normal with only minimal lymphangiectasia in biopsies. Further evaluations revealed an indolent marginal zone lymphoma with minor bone marrow infiltration. Monotherapy with rituximab decreased bone marrow infiltration of the lymphoma but did not relieve PLE. Additional treatments with steroids, octreotide, a diet devoid of long-chain fatty-acids, and parenteral nutrition did not prevent further clinical deterioration with marked weight loss (23 kg), further reduction in albumin concentrations (nadir 8 g/L), and a pronounced drop in performance status. Finally, immunochemotherapy with rituximab and bendamustine resulted in hematological remission and remarkable clinical improvement. 18 months after therapy the patient remains free of gastrointestinal complaints and has regained his body weight with normal albumin levels. We demonstrate a case of PLE secondary to indolent marginal zone lymphoma. No intestinal pathologies were detected, contrasting a severe and almost lethal clinical course. Immunochemotherapy relieved lymphoma and PLE, suggesting that a high suspicion of lymphoma is warranted in otherwise unexplained cases of PLE.

67-OR

Objectives The KDIGO 2012 criteria emphasize the independent role of glomerular filtration rate (GFR) and albuminuria to assess the prognosis of chronic kidney disease (CKD), as both relate independently to all-cause mortality and cardiovascular morbidity/mortality. In this study we want to determine the prevalence of CKD in women with a recent history of preeclampsia. Methods We included 602 primiparous women with a history of preeclampsia. They were all at least 4 months postpartum and had no history of pre-existent hypertension, diabetes or kidney disease. We estimated GFR by the CKD-epi-equation, and quantified urinary protein loss (micro-albuminuria: >3.0 mg/mmol creatinine; macro-albuminuria: proteinuria >300 mg/24 h). We categorized women on the basis of the KDIGO 2012 criteria. Results Median time postpartum was 9 (6–18) months. Table 1 shows the different GFR and albuminuria categories. 419 (70%) women had a normal GFR and no albuminuria. Based on the KDIGO guideline, 77 (13%) women with a moderately increased risk would require yearly monitoring, in over 85% of the cases because of excessive urinary protein loss. Only 21 (3.5%) women were classified to be at high risk and would require referral to a nephrologist for twice yearly monitoring. Conclusions Follow-up of kidney function is relevant for about 16% of all women with a history of preeclampsia. Kidney function should be part of cardiovascular risk assessment after preeclampsia, with special emphasis to be directed on the postpartum disappearance of the preeclampsia-induced albuminuria. Disclosures J. Spaan: None. V. Lopez van Balen: None. L. Peeters: None. M. Spaanderman: None.

Review of Commonly Used Clinical Pathology Parameters for General Gastrointestinal Disease with Emphasis on Small Animals

A wide variety of markers are available to assess the function and pathology of the gastrointestinal (GI) tract. This review describes some of these markers with special emphasis given to markers used in dogs and cats. Small intestinal disease can be confirmed and localized by the measurement of serum concentrations of folate and cobalamin. Fecal α1-proteinase inhibitor concentration can increase in individuals with excessive GI protein loss. A wide variety of inflammatory markers are available for a variety of species that can be used to assess the inflammatory activity of various types of inflammatory cells in the GI tract, although most of these markers assess neutrophilic inflammation, such as neutrophil elastase, calprotectin, or S100A12. N-methylhistamine can serve as a marker of mast cell infiltration. Markers for lymphocytic or eosinophilic inflammation are currently under investigation. Exocrine pancreatic function can be assessed by measurement of serum concentrations of pancreatic lipase immunoreactivity (PLI) and trypsin-like immunoreactivity (TLI). Serum PLI concentration is increased in individuals with pancreatitis and has been shown to be highly specific for exocrine pancreatic function and sensitive for pancreatitis. Serum TLI concentration is severely decreased in individuals with exocrine pancreatic insufficiency.

English

Abstract Introduction Intestinal lymphangiectasia is a protein-losing enteropathy caused by congenital malformation or secondary obstruction of intestinal lymphatic vessels, which usually causes excessive protein loss in the intestine and malabsorption syndrome. Patients may be asymptomatic or complain of oedema, diarrhoea, hypoalbuminaemia and other deficiencies. This article reports a case of chronic diarrhoea and an abdominal mass. Case report We present the case of a 70-year-old woman who came to our gastroenterological clinic for diarrhoea. Blood and stool tests were within the normal ranges, except for a mild eosinophilia and a high C-reactive protein. The ultrasound scan showed a cystic retropancreatic mass, and the following computed tomography scan confirmed the presence of the mass without sure continuity with the dorsal pancreas. The fine needle aspiration performed during an echoendoscopy, permitted the complete aspi ration of the fluid and the cytological analysis that showed numerous lymphocytes. The diagnosis of Intestinal lymphangiectasia was done, and Chronic diarrhoea and abdominal mass: a case of intestinal lymphangiectasia

Successful treatment of protein-losing enteropathy due to AA amyloidosis with octreotide in a patient with rheumatoid arthritis

Protein-losing enteropathy (PLE) is a rare syndrome of gastrointestinal protein loss that may complicate a variety of diseases. This excessive protein loss across the gut epithelium can be explained by several mechanisms, such as augmentation of the intestinal mucosal capillary permeability, mucosal disruption, intestinal or mesenteric vasculitis, and lymphangiectasia. However, these pathophysiologic alterations of the gut are closely linked to the underlying cause, and primary treatment for PLE should be directed at the underlying condition. Here, we report a female patient with rheumatoid arthritis who developed severe PLE due to AA amyloidosis and was successfully treated with octreotide. She had been suffered from rheumatoid arthritis for 18 years, and her arthritic symptoms at the time of presentation were not definite but manifested as severe diarrhea and general edema with hypoalbuminemia. PLE due to gastrointestinal amyloidosis was confirmed by increased fecal α1-antitrypsin clearance and a colonoscopic biopsy that was positive for amyloid deposits. The diarrhea dissipated with conventional treatment, but the general edema resolved only after introducing a long-acting somatostatin analog (octreotide), along with a gradual recovery of the serum albumin level. This case teaches us that in the case of PLE due to AA amyloidosis that is refractory to conventional treatment, the administration of octreotide should be considered.