Degree Of Renal Failure Research Articles

Best use of cardiac biomarkers in patients with AL amyloidosis and renal failure

In AL amyloidosis prognosis depends on the severity of heart dysfunction which is best assessed by natriuretic peptides (BNP and NT-proBNP). However, their clearance relies on glomerular filtration rate (GFR) and their concentration increases with renal failure. We evaluated the diagnostic and prognostic performance of NT-proBNP and BNP in 248 patients with AL amyloidosis with different degrees of renal failure. Patients were grouped according to GFR. Group 1 comprised 109 patients with GFR ≥60 mL/min/1.73 m(2) , Group 2, 77 subjects with GFR <60 and ≥15 mL/min/1.73 m(2) , and Group 3, 62 patients with GFR <15 mL/min/1.73 m(2) . The ability of natriuretic peptides to detect heart involvement and to predict survival in the three groups was assessed. Decreasing eGFR required higher cutoffs of both NT-proBNP and BNP for detecting heart involvement and predicting survival. Both natriuretic peptides were independent prognostic markers in Groups 1 and 2, whereas in Group 3 only BNP independently predicted survival. Natriuretic peptides are powerful and useful markers of cardiac dysfunction and prognosis, provided that eGFR is considered in interpreting their clinical meaning. BNP should be preferred in patients with end-stage renal failure.

The use of newer antiepileptic drugs in patients with renal failure

Seizures and chronic kidney disease are both common and often coexist. Treating seizures in patients with renal failure, including those on dialysis, is a challenge that is frequently encountered, especially in the inpatient setting. For the newer antiepileptic drugs, there are limited data available, so an understanding of how each drug is affected by kidney disease and dialysis is critical in order to make rational choices qualitatively (which drug) and quantitatively (dosing). Generally, newer (second-generation) antiepileptic drugs are associated with fewer systemic side effects and drug–drug interactions, so they tend to be preferred in this population. The landscape of antiepileptic drugs is constantly evolving, with new compounds being released on a regular basis. Thus, several new agents have become available since the last review of this topic (in 2006) and these are the ones discussed here. Most require dosage adjustment according to the degree of renal failure, and most require extra doses after dialysis.

Rituximab Treatment for Membranous Nephropathy: A French Clinical and Serological Retrospective Study of 28 Patients

The development of well-tolerated and effective therapies that target the pathogenesis of membranous nephropathy (MN) would be useful. Our objective was to evaluate the efficacy of rituximab in MN. We analyzed the outcome of 28 patients treated with rituximab for idiopathic MN. Anti-PLA₂R antibodies in serum and PLA₂R antigen in kidney biopsy were assessed in 10 and 9 patients, respectively. Proteinuria was significantly decreased by 56, 62 and 87% at 3, 6 and 12 months, respectively. At 6 months, 2 patients achieved complete remission (CR) and 12 partial remission (PR; overall renal response, 50%). At 12 months (n = 23), CR was achieved in 6 patients and PR in 13 patients (overall renal response, 82.6%). Three patients suffered a relapse of nephrotic proteinuria 27–50 months after treatment. Univariate analysis suggested that the degree of renal failure (MDRD estimated glomerular filtration rate <45/ml/min/1.73 m²) is an independent factor that predicts lack of response to rituximab. Anti-PLA₂R antibodies were detected in the serum of 10 patients, and PLA₂R antigen in immune deposits in 8 of 9 patients. Antibodies became negative in all 5 responsive patients with available follow-up sera. In this retrospective study, a high rate of remission was achieved 12 months after treatment.

Calcium-alkali syndrome in post-surgical hypoparathyroidism

Milk-alkali syndrome or its up-to-date definition ‘calcium-alkali syndrome’ (CAS),1 is characterized by the triad of hypercalcemia, metabolic alkalosis and various degrees of renal failure, due to the intake of variable amounts of calcium and absorbable alkali. Its initial description dates back to the early 20th century when ‘alkali powders’ became a popular therapy for peptic ulcer disease.2 In 1923, two researchers from the Mayo Clinic, Leo Hardt and Andrew Rivers,3 described the adverse effects of this treatment, and in the three following decades communications about toxicity of Sippy's protocol were frequent.4 CAS has become a rare cause of hypercalcemia (<1% of cases) since proton pump inhibitor therapy was introduced in the 1990s.5,6 Nevertheless, it remains the third most common cause of hypercalcemia and the second most frequent cause of severe hypercalcemia among inpatients.5 The main reason for the rise of incidences of CAS is the increase of calcium carbonate use for prophylaxis and treatment of osteoporosis in post-menopausal women. Notably, any situation in which an overload of calcium and alkaline element coexist fosters a risk for CAS. We describe three patients who developed this syndrome in the setting of a post-surgical hypoparathyroidism. ### Case 1 A 71-year-old woman was admitted to our hospital with a 10-day history of nicturia, polyuria, fatigue, nervousness, insomnia and headache. Her past medical history included hypertension, treated with lisinopril and hydrochlorothiazide (20/12.5 mg/day), mild chronic renal failure (creatinine, 1.6 mg/dl) and primary hyperparathyroidism. She had undergone total thyroidectomy and parathyroid resection 2 years earlier and required a second intervention 1 year later because of a new mediastinal parathyroid adenoma. At the time she developed permanent post-operative hypothyroidism and hypoparathyroidism, and calcium carbonate (900 mg/day), calcitriol (1 µg/day) and levothyroxine (100 µg/day) were started. At admission laboratory results were as follows: serum creatinine, 2.4 mg/dl; urea, 104 mg/dl; …

Opioid-Induced Neurotoxicity in the Hospice Patient

A potential adverse effect of opioids in the hospice patient is a condition called opioid-induced neurotoxicity. It is a syndrome characterized by symptoms such as severe pain, tremors, seizures, confusion, and hallucinations and is easily missed by unaware clinicians. Hospice patients are particularly at risk because of high doses of opioids and some degree of renal failure. Retained opioid metabolites may cause neuroexcitatory and antianalgesic adverse effects. In this instance, the opioids can be a cause of patient suffering. As pain levels increase, the instinct of the provider is to increase the dose of the opioid. Unfortunately, this augments the pool of metabolites and further amplifies the symptoms. This in turn may lend to cyclical increases in opioid doses by well-meaning healthcare professionals. This article examines recent evidence-based literature regarding opioid-induced neurotoxicity and discusses clinical implications for nurses who care for the terminally ill. Key points of assessment and a framework of management strategies are provided to aid in effective symptom management.

Symptomatic Capillaria plica infection in a young European cat

An 8-month-old owned European cat showing abdominal pain, fever, distended painful bladder and urinary blockage was presented. Intravenous fluids were immediately administered and, after sedation, a urinary catheter was applied. Blood and urine analysis revealed cystitis and a moderate-to-severe degree of renal failure. About 20 thread-like nematodes, identified as Capillaria plica larvae and fragments of adult stages, were found in the urine sediment. After treatment with an oral formulation of fenbendazole at 25 mg/kg q 12 h for 10 days, urinary signs and bladder worms disappeared. Cases of Capillaria species bladder worms in cats are rarely reported and most infected cats show no clinical signs, presumably because of a low parasite burden. In the present study, feline capillariosis was associated to urethral obstruction, severe difficulties in urination, cystitis and renal failures.

Matrix Gla Protein Metabolism in Vascular Smooth Muscle and Role in Uremic Vascular Calcification

Matrix Gla protein (MGP) is an inhibitor of vascular calcification but its mechanism of action and pathogenic role are unclear. This was examined in cultured rat aortas and in a model of vascular calcification in rats with renal failure. Both carboxylated (GlaMGP) and uncarboxylated (GluMGP) forms were present in aorta and disappeared during culture with warfarin. MGP was also released into the medium and removed by ultracentrifugation, and similarly affected by warfarin. In a high-phosphate medium, warfarin increased aortic calcification but only in the absence of pyrophosphate, another endogenous inhibitor of vascular calcification. Although GlaMGP binds and inactivates bone morphogenic protein (BMP)-2, a proposed mediator of vascular calcification through up-regulation of the osteogenic transcription factor runx2, neither warfarin, BMP-2, nor the BMP-2 antagonist noggin altered runx2 mRNA content in aortas, and noggin did not prevent warfarin-induced calcification. Aortic content of MGP mRNA was increased 5-fold in renal failure but did not differ between calcified and noncalcified aortas. Immunoblots showed increased GlaMGP in noncalcified (5-fold) and calcified (20-fold) aortas from rats with renal failure, with similar increases in GluMGP. We conclude that rat aortic smooth muscle produces both GlaMGP and GluMGP in tissue-bound and soluble, presumably vesicular, forms. MGP inhibits calcification independent of BMP-2-driven osteogenesis and only in the absence of pyrophosphate, consistent with direct inhibition of hydroxyapatite formation. Synthesis of MGP is increased in renal failure and deficiency of GlaMGP is not a primary cause of medial calcification in this condition.

Marcadores cardiacos en diferentes grados de enfermedad renal crónica: influencia de la inflamación y de la afectación cardiaca previa

Background and objectiveTroponin T (TnT), brain natriuretic peptide (BNP) and its precursor (NT-proBNP) are useful markers of acute coronary events and heart failure. The aim of this study was to analyze the influence of chronic renal failure, inflammation and heart disease in these biomarkers. Patients and methodsIn 266 patients with different stages of chronic renal diseases, the following parameters were measured: cardiac markers (TnT, BNP and NT-proBNP), renal function, inflammatory markers (hsCRP, fibrinogen, albumin, uric acid and white blood cells). We recorded the cardiovascular history. Ventricular dysfunction and left ventricular hypertrophy were assessed by echocardiography. ResultsA significant correlation between cardiac markers and inflammatory parameters such as fibrinogen, hsCRP and albumin was found. Age (OR 1.05, P = .021), serum albumin (OR: 0.06, P=.006), ischemic heart disease (OR: 8.17, P=.0092) and renal failure (OR: 1.67, P=.05) were predictors of higher BNP levels. Age (OR 1.05, P=.0097), serum albumin (OR: 0.12, P=.001), ischemic heart disease (OR: 3.43, P=.034), renal failure (OR: 1, 65, P=.036) and heart failure (OR: 4.33, P=.0312) were predictors of elevated NT-proBNP. Previous ischemic heart disease alone increased TnT levels (OR: 6.51, P=.0012). ConclusionsAge, previous cardiac disease and inflammation increase cardiac marker levels in patients with different stages of renal disease, but the degree of renal failure is an important factor influencing NT-proBNP levels. However, ischemic heart disease alone increases the levels of TnT.

Gonadal dysfunction in men with chronic kidney disease: clinical features, prognostic implications and therapeutic options

Gonadal dysfunction is a frequent finding in men with chronic kidney disease and with end-stage renal disease. Testosterone deficiency, usually accompanied by elevation of serum gonadotropin concentrations, is present in 26-66% of men with different degrees of renal failure. Uremia-associated hypogonadism is multifactorial in its origin, and rarely improves with initiation of dialysis, although it usually normalizes after renal transplantation. Experimental and clinical evidence suggests that testosterone may have important clinical implications with regards to kidney disease progression, derangements in sexual drive, libido and erectile dysfunction, development of anemia, impairment of muscle mass and strength, and also progression of atherosclerosis and cardiovascular disease. Additionally, low testosterone levels in hemodialysis patients have been associated with increased mortality risk in some studies. Currently, we count with available therapeutic options in the management of uremic hypogonadism, from optimal delivery of dialysis and adequate nutritional intake, to hormone replacement therapy with different testosterone preparations. Other potential options for treatment include the use of antiestrogens, dopamine agonists, erythropoiesis-stimulating factors, vitamins, essential trace elements, chorionic gonadotropin and renal transplantation. Potential adverse effects of androgen replacement therapy in patients with kidney disease comprise, however, erythrocytosis, prostate and breast cancer growth, reduced fertility, gynecomastia, obstructive sleep apnea and fluid retention. Androgen preparations should be used with caution with stringent monitoring in uremic men. Although there are encouraging data suggesting plausible benefits from testosterone replacement therapy, further studies are needed with regards to safety and effectiveness of this therapy.

A Rare Case of Thrombotic Thrombocytopenic Purpura Presenting With Pancreatitis

Thrombotic thrombocytopenic purpura (TTP) is a rare disease characterized by platelet consumption in thromboses, leading to a microangiopathic hemolytic anemia (MAHA). Thrombotic thrombocytopenic purpura involves a decrease in the activity of a metalloproteinase, ADAMTS13, which is critical in regulation of the coagulation cascade. This occurs in several conditions, and therefore, TTP is associated with a number of diseases. The decreased activity of ADAMTS13 leads to occlusive platelet thrombi, which can result in a variety of tissue manifestations. Patients normally present with nonspecific symptoms, such as fever and petechia. The classic pentad, although now extraordinarily uncommon, includes thrombocytopenia, MAHA, varying degrees of renal failure, fever, and nonlocalizable neurologic symptoms. We present a rare case in which pancreatitis was the presenting condition in a patient with acute idiopathic TTP. We discuss the pathogenesis and etiologies of these 2 diseases.

RENAL VEIN THROMBOSIS WITH PULMONARY EMBOLISM: FIRST MANIFESTATION OF LUPUS NEPHRITIS

RENAL VEIN THROMBOSIS WITH PULMONARY EMBOLISM: FIRST MANIFESTATION OF LUPUS NEPHRITIS

Steady state pharmacokinetics and dose equivalents of oral clodronate in renal failure

Clodronate is used in the treatment of osteoporosis, and malignancy-associated bone disease. The steady state pharmacokinetics and the dose equivalents of oral clodronate were assessed in subjects with various degrees of renal failure. 1,600 mg of clodronate was given orally mornings for 11 days to 14 healthy volunteers (creatinine clearance, CLCr, > 80 ml/min), and 18, 12 and 16 subjects with mild (50 - 80 ml/min), moderate (30 - 50 ml/min) and severe (< 30 ml/min) renal failure, respectively. Trough drug levels at 4, 7 and 11 days, and concentration-time curves for 72 h after the last dose were followed. In all study groups, the trough drug levels achieved the kinetic steady state within 11 days. The area under the 24-h concentration-time curve (AUC0-24) enlarged and the elimination half-life (t1/2elim) prolonged progressively when the renal function was impaired. The maximum drug level and the time to maximum were not changed significantly in the renal failure. In the steady state phase, the diurnal drug excretion (E0-24) was not changed by the kidney function, but the renal drug clearance (CLD) decreased in close correlation with CLCr. The normal-to-failed AUC0-24 ratios in mild, moderate, and severe renal failure were 0.53, 0.43 and 0.31, respectively, when the ideally-matched counterpart was assumed as the normal reference to each renal failure group. In mild, moderate and severe renal failure, 53%, 43% and 31% oral clodronate doses, respectively, resulted in drug AUCs similar to those in controls with normal (> 80 ml/min) CLCR.

Elección del agente oral más apropiado, en monoterapia o en combinación, en el paciente anciano con diabetes

The elderly patient with diabetes presents a series of features that we need to have in mind when considering drug therapy, such as quality of life, presence of chronic complications, major geriatric syndromes, and patient preferences. The limited evidence available due to the few studies performed in the elderly explains the limited existing recommendations in the most current clinical practice guidelines. Metformin is the drug of choice as monotherapy and its dosage should be adjusted to the degree of renal failure, a situation very common in the elderly. Other pharmacologic groups can also be used taking into account their limitations and contraindications. There is no consensus on what is the most appropriate combination therapy in the elderly when monotherapy fails. Any combination can be used provided that the indications and contraindications are considered. When insulin is necessary, benefits and risks of using insulin should be evaluated, using the simplest regimen adapted to the characteristics of the elderly and its environment.

La profilassi della tromboembolia venosa nei pazienti con malattia renale cronica

Summary Despite the high morbidity and mortality associated with venous thromboembolism in hospitalized medical patients with a number of risk factors, and large evidence that prophylaxis is effective, prophylaxis rates remain elusive in medically ill patients. Furthermore, in patients with renal failure, prophylaxis often is omitted or sub-optimal, due to fear of provoking hemorrhage. Patients with end-stage renal disease often have platelet deficits. Low molecular weight heparin (LMWH) therapy may also be difficult to manage in these cases because LMWH clearance is largely dependent on the kidneys. Administration of LMWH to patients with some degree of renal failure may lead to bioaccumulation of anti-Xa activity with an increased risk of bleeding. In recent years, LMWH has largely replaced unfractionated heparin (UFH) for the treatment and prophylaxis of thromboembolic disease. LMWHs have been shown to be superior to UFH in the prevention of venous thromboembolism. They are also easier to administer and do not require laboratory monitoring. However, several case reports and a meta-analysis indicate that the use of LMWHs at therapeutic doses in patients with advanced renal failure can be associated with major bleeding with serious adverse effects. In this paper, we review recent evidence supporting the safety of LMWHs at prophylactic doses in patients with mild or moderate renal disease. Current evidence suggests that bioaccumulation of enoxaparin (the most widely used LMWH) can occur when the drug is used at standard therapeutic doses in patients with severely impaired renal function. This risk can be reduced by empiric dose reduction or monitoring of anti-Xa heparin levels.

Phosphate: despite advances in research, the benefits to patients remain limited

Tremendous progress has been made over recent years in the understanding of the mechanisms regulating calcium, phosphorus, vitamin D, and parathyroid hormone homeostasis in the normal human body and in patients with different degrees of renal failure. In addition, some of these findings have been translated into clinical practice, be it diagnostic or therapeutic.

Selenium, Lead, and Cadmium Levels in Renal Failure Patients in China

Whole blood and serum samples of Chinese stable chronic renal failure (CRF) patients (n = 81), hemodialysis patients (n = 135), posttransplant patients (n = 60), and subjects with normal renal function (NRF; N = 42) were collected, as well as water and dialysate samples from five dialysis centers. The concentration of selenium (Se), lead (Pb), and cadmium (Cd) was measured by atomic absorption spectrometry. The mean serum Se levels in patients with different degrees of renal failure were significantly lower than those of subjects with NRF (p < 0.01). Pb levels were not increased in renal failure patients, while the Cd levels in patients with various degrees of renal failure were higher than in subjects with NRF (p < 0.05). After correcting the results of Pb and Cd for hematocrit (Hct) however, Pb levels of dialysis patients were also increased. In the dialysis population under study, blood Pb and Cd levels were closely related to the time on dialysis, while contamination of the final dialysate may also contribute to the increased blood Cd and to a less extent Pb levels. Correction for Hct may be recommended to accurately compare blood Pb and Cd levels in dialysis patients and CRF patients with varying degrees of anemia to those of subjects with NRF.

Milk-alkali syndrome.

Milk-alkali syndrome (MAS) consists of hypercalcemia, various degrees of renal failure, and metabolic alkalosis due to ingestion of large amounts of calcium and absorbable alkali. This syndrome was first identified after medical treatment of peptic ulcer disease with milk and alkali was widely adopted at the beginning of the 20th century. With the introduction of histamine2 blockers and proton pump inhibitors, the occurrence of MAS became rare; however, a resurgence of MAS has been witnessed because of the wide availability and increasing use of calcium carbonate, mostly for osteoporosis prevention. The aim of this review was to determine the incidence, pathogenesis, histologic findings, diagnosis, and clinical course of MAS. A MEDLINE search was performed with the keyword milk-alkali syndrome using the PubMed search engine. All relevant English language articles were reviewed. The exact pathomechanism of MAS remains uncertain, but a unique interplay between hypercalcemia and alkalosis in the kidneys seems to lead to a self-reinforcing cycle, resulting in the clinical picture of MAS. Treatment is supportive and involves hydration and withdrawal of the offending agents. Physicians and the public need to be aware of the potential adverse effects of ingesting excessive amounts of calcium carbonate.

Immunofluorescence staining for the detection of immunoglobulins and complement (C3) in dogs with renal disease

Renal cortical biopsies from 74 dogs with different degrees of renal failure were studied by immunofluorescence to assess the frequency and extent of the deposition of immunoglobulins G, M and...

Is bowel preparation before colonoscopy a risky business for the kidney?

Acute phosphate nephropathy after bowel preparation with oral sodium phosphate (OSP) for colonoscopy has emerged as an important clinical entity. In 2004, five cases of nephrocalcinosis and irreversible renal failure after bowel preparation with OSP were reported. More recently, several retrospective studies have shown that the incidence of acute kidney injury after OSP use is in the range of 1-4%, similar to the incidence of contrast nephropathy in the general population. The degree of renal failure is not generally as severe as in the first reported cases, but irreversible damage can still occur. Millions of people worldwide undergo screening colonoscopies for colon and rectal cancer after the age of 50, so careful patient selection and monitoring for possible complications is essential when OSP is used. In addition to educating patients about the possibility of renal damage, physicians should routinely watch for considerable weight loss during bowel preparation and correct the fluid deficit as needed. Carrying out a renal function panel, which includes serum phosphorus level, is prudent after colonoscopy. Alternative bowel cleansing agents are needed because calcium phosphate precipitation is inevitable after OSP use even in the normal kidney.

Insulin therapy in renal disease

Diabetes mellitus (DM) is the main cause of end-stage renal disease (ESRD). Conversely, chronic renal failure (CRF) is also associated with diverse alterations in carbohydrate and insulin metabolism. CRF-induced metabolic disorders should be borne in mind when treating diabetic patients, to ensure the introduction of adequate therapy adjustments that are in line with the onset of renal function decline. Moreover, several specific therapies employed in CRF may also influence pharmacological therapy of DM in uraemic patients. Adequate glycaemic control has also been associated with a reduction in the onset and progression of diabetic nephropathy as well as in the morbidity and mortality in uraemic diabetic patients during dialysis. Intensive insulin therapy can notably improve glycemic control and it should be considered part of the management of insulin-treated CRF diabetic patients. Insulin analogues have been recently evaluated in CRF diabetic patients, with encouraging results. In this study, we review the more relevant aspects related to insulin therapy in diabetic patients with different degrees of renal failure and in patients with ESRD, both in conservative therapy and dialysis.