Chronic Renal Parenchymal Disease Research Articles

Sonographically Determined Renal Size and Echogenicity as a Predictor of Chronic Irreversible Renal Parenchymal Disease in Glomerulonephritis Patients: Comparison with Histopathology

Sonographically Determined Renal Size and Echogenicity as a Predictor of Chronic Irreversible Renal Parenchymal Disease in Glomerulonephritis Patients: Comparison with Histopathology

BILATERAL RENAL ARTERY EMBOLIZATION IN END-STAGE RENAL DISEASE AND RESISTANT HYPERTENSION

Objective: Some patients with end-stage renal disease present with resistant or refractory arterial hypertension despite dialysis and use of multiple antihypertensive drugs. Renal artery embolization is a rarely used minimally invasive interventional procedure which may provide improved blood pressure (BP) control in chronic renal parenchymal disease by eliminating renal function while avoiding the morbidity and mortality of a nephrectomy. Design and method: A 44-year old white male with chronic glomerulonephritis and stage 5 chronic kidney disease undergoing regular dialysis treatment was referred for refractory arterial hypertension. Despite treatment by 7 antihypertensive drugs and good therapeutic adherence his office and ambulatory BP remained very high. Plasma renin was markedly elevated and CT angiography found diffuse atherosclerotic changes of renal arteries. Sequential catheter-based renal artery embolization with application of a tissue glue was indicated. Results: In September 2019, catheter based embolization of right renal artery was performed in analgosedation, followed by the embolization of the left renal artery two weeks later. Because of the rapid antihypertensive effect of the procedure, antihypertensive medications were reduced at the time of the left-sided procedure (from 9 to 6 defined daily doses). One month after the renal artery embolization, despite reduced medication, office BP decreased from baseline 170/106 mmHg by 57/22 mmHg. Mean 24-hour, day-time and night-time ambulatory BP was reduced by 15/11 mmHg, 14/11 and 34/15 mmHg, respectively. The patient reported prolonged flank pain lasting approximately one week after the embolization, which responded well to conventional analgesics. Conclusions: Renal artery embolization lead to a marked improvement of BP control in a patient with end-stage renal disease, refractory arterial hypertension and high plasma renin. Further studies are warranted to assess the efficacy and safety of renal artery embolization in such patients.

Alteration in different lipoprotein fractions in chronic renal failure patients

Background: Chronic renal failure, which is an inevitable terminal pathway of any chronic renal parenchymal disease, is more known for its morbidity than for its mortality. Objective: To note the alteration in different lipoprotein fractions among chronic renal failure patients. Methods: 70 Cases of chronic renal failure were taken for study. These patients were divided into two groups of 35 each. One group consisting of 35 Patients who were on conservative treatment, and the other group of 35 patients were on regular short term hemodialysis (6 months – 2 years). Patients were selected from Kasturba Medical College Hospitals and from Wenlock Government Hospital, Mangalore, from April 2001 to December 2003. Results: The HDL – cholesterol level was found to be significantly lower compared to control group. The total cholesterol and LDL was not raised significantly. The HDL/TC ratio was significantly reduced. Conclusion: Significant rise in triglyceride and VLDL concentration was seen in chronic renal failure patients.

Secondary hypertension: Obstructive sleep apnea

In patients with hypertension and chronic renal parenchymal disease, BP should be controlled to 130/85 mmHg or lower (125/75 mmHg) in patients with proteinuria in excess of 1 g/day. Reducing dietary sodium (< 7 g/day) and protein (< 0.6-0.7 g/kg) helps control high BP and renal function in patients with renal insufficiency. As first antihypertensive drug, ACE inhibitors or long-acting Ca antagonists are recommended. In patients with renovascular hypertension, angioplasty is the first choice increasingly to be accompanied by stenting, and surgical revascularization is the next choice. As antihypertensive drugs, beta blockers, ACE inhibitors, and AII-receptor blockers are recommended. Hypertension accompanied by endocrine disease with adenoma or tumor is almost cured or improved by surgical removal. Spironolactone and Ca antagonists are used in patients with idiopathic aldosteronism (bilateral hyperplasia). Alpha and beta blockers are used in patients with pheochromocytoma during preoperative period.

Beta-Thalassemia Minor Is Associated with IgA Nephropathy

Jung Hyun Kang, M.D., Bo Rha Park, M.D., Kyung Soo Kim, M.D., Do Yeun Kim, M.D., Hee Jin Huh, M.D., Seok Lae Chae, M.D., and Sung Joon Shin, M.D.. Ann Lab Med 2013;33:153-5. https://doi.org/10.3343/alm.2013.33.2.153

Renal dysfunction in acute and chronic heart failure: prevalence, incidence and prognosis

Most patients with heart failure have mild or moderate renal dysfunction. This reflects the combined impact of chronic renal parenchymal disease, renal artery disease, renal congestion and hypoperfusion, neuroendocrine and cytokine activation and the effects of treatments for heart failure. Remarkably, with good treatment, the average annual rate of decline in renal function is similar in patients with chronic heart failure and healthy people of a similar age. Urea appears to be a stronger marker of an adverse prognosis than creatinine-based measures of renal function. Recent evidence suggests that minor, transient increases in creatinine in the setting of acute heart failure are not prognostically important but persistent deterioration does indicate a higher mortality. The poor prognosis of patients with worsening renal function ensures that few require renal dialysis but this may change as methods to prevent sudden death improve and new ways are found to control fluid congestion. Reversing renal dysfunction and stopping its progression remain important targets for treatment of heart failure.

Screening for Microalbuminuria in HIV-Positive Children in Enugu

Background. Human immunodeficiency virus associated nephropathy (HIVAN) is a rapidly progressive chronic renal parenchymal disease that occurs in HIV-infected individuals and manifests commonly as proteinuria, which is preceded by microalbuminuria (MA). This clinical entity is defined as a spot urine albumin of 20–200 mg/L. Objectives. To determine the prevalence of microalbuminuria in HIV positive children in UNTH, Enugu and compare it with that of HIV-negative children. Methods. A total of 154 HIV positive children aged 18 months to 14 years and 154 HIV-negative children of corresponding attributes were screened for microalbuminuria, using Micral test II strip which has a sensitivity of 90–99%. Results. No child among the groups (HIV positive and negative) had microalbuminuria. Majority (96.0%) of HIV-positive children had nonadvanced HIV disease at the time of the study (P = 0.00). About 77.3% were using HAART (P < 0.0001), the mean CD4 cell count of the subjects was 709.2 ± 443.9 cells/mm3; while 78.0% had nonsevere immunosuppression (P = 0.00). Furthermore, HIV-positive children with severe immunosuppression were younger and had shorter duration of treatment. Conclusion. Microalbuminuria may not be very common in Nigerian children irrespective of their HIV status.

Systemic Hypertension and Proteinuria in Childhood Chronic Renal Parenchymal Disease

A variety of chronic kidney diseases tend to progress towards end-stage kidney disease. Progression is largely due to factors unrelated to the initial disease, including systemic hypertension and proteinuria. Drugs that block the renin-angiotensin II-aldosterone system, either ACE inhibitors or angiotensin II receptor antagonists, reduce both BP and proteinuria and appear superior to a more conventional antihypertensive treatment regimen in preventing progression to end-stage kidney disease. The most recent recommendations state that the BP goal in children with chronic kidney disease is the corresponding 90th centile for body height, age, and gender. Since satisfactory BP control is often not achieved, the mnemonic acronym DELTAREPROSI was generated to recall the following tips for the practical management of hypertension and proteinuria in childhood chronic renal parenchymal disease: DEfinition of hypertension and Low blood pressure TArget in REnal disease (90th centile calculated by means of simple formulas), potential of drugs inhibiting the REnin-angiotensin II-aldosterone system in hypertension and PROteinuria, advantages of SImplified treatment regimens and escalating the doses every SIx weeks.

Effect of efonidipine and ACE inhibitors on proteinuria in human hypertension with renal impairment

Background Although several lines of recent studies fail to demonstrate the beneficial action of calcium antagonists, a novel dihydropyridine efonidipine, which possesses dilatory action of both afferent and efferent arterioles and, therefore, shares the renal microvascular action with angiotensin converting enzyme (ACE) inhibitors, is reported to exhibit renal protection in experimental animals. Methods The present study evaluated the effect of efonidipine and ACE inhibitors on blood pressure (BP) and proteinuria. Sixty-eight hypertensive patients with renal impairment (serum creatinine, >1.5 mg/dL) or chronic renal parenchymal disease were randomly assigned to efonidipine or ACE inhibitor treatment. Of the 68 patients, 23 were treated with efonidipine and 20 with ACE inhibitors; these patients were analyzed for the 48-week study. Results Both efonidipine and ACE inhibitors produced a similar degree of reductions in BP (efonidipine, from 161 ± 2/93 ± 2 to 142 ± 5/82 ± 2 mm Hg; ACE inhibitor, from 163 ± 3/95 ± 2 to 141 ± 5/83 ± 2 mm Hg), and maintained creatinine clearance for 48 weeks. Proteinuria tended to decrease in both groups, and a significant reduction was observed in proteinuric patients (>1 g/day) (efonidipine, from 2.7 ± 0.3 to 2.1 ± 0.3 g/day; ACE inhibitor, from 3.0 ± 0.4 to 2.0 ± 0.5 g/day). Of interest, efonidipine decreased proteinuria in proteinuric patients who failed to manifest decreases in systemic BP. Finally, the incidence of adverse effects, including hyperkalemia and cough, was less in the efonidipine-treated group. Conclusions Both efonidipine and ACE inhibitors preserved renal function in hypertensive patients with renal impairment. The antiproteinuric effect was apparent in patients with greater proteinuria. The beneficial action of efonidipine, along with fewer side effects, may favor the use of this agent in the treatment of hypertension with renal impairment.

Slowing the Progression of Chronic Renal Parenchymal Disease

End-stage renal failure (ESRF) is a major cause of morbidity and mortality in North America as well as in the rest of the world. In addition, the treatment of patients who have ESRF is quite expensive. It is estimated that for an in-hospital hemodialysis patient, the average annual cost is approximately $54,000 in Canadian dollars and a peritoneal dialysis patient's annual care costs approximately $32,000 in Canadian dollars, whereas a kidney transplant patient costs about $25,000 dollars a year in Canadian dollars. And as renal replacement therapy by hemodialysis, periltoneal dialysis or successful kidney transplantation prolongs survival in ESRF patients, new dialysis patients have been outnumbering those who die from ESRF. To complicate matters further, the number of ESRF patients have been on the rise the last two decades and is expected to continue to rise at a rate of about 6 to 10% per year through the next one to two decades, putting more strain on the national economy, human resources and on an already strained health care system. Therefore, it makes sense to slow down or delay the progression of chronic renal parenchymal disease, or when possible, to prevent it from happening altogether. In this article, we will review the mechanisms and course of progression of renal injury and elaborate on the currently recommended strategies to delay or halt the progression of chronic renal disease.

RENAL DOPAMINERGIC MECHANISMS IN RENAL PARENCHYMAL DISEASES, HYPERTENSION, AND HEART FAILURE

The recovery of renal function in renal transplant recipients is accompanied by an enhanced ability to synthesize dopamine (DA), which may contribute to maintain sodium homeostasis. Patients suffering from chronic renal parenchymal disease, a well-recognized form of salt sensitive (SS) hypertension, have a reduced ability to produce DA that correlates well with deterioration of renal function. In patients afflicted with IgA nephropathy, but normal renal function, urinary excretion of DA correlated positively with BP responses to changes from 200 to 20 mmol/day salt intake. In black salt resistant (SR) normotensives (NT) and SR hypertensives, under low salt intake (40 mmol/day), but not SS-NT and SS-HT, the saline infusion induced increments of DA and DOPAC urinary excretion correlated significantly with increments of sodium urinary excretion and sodium fractional excretion. Patients afflicted with heart failure (HF) have a reduced delivery of L-DOPA to the kidney, accompanied by an increase in DA/L-DOPA urinary ratios. This suggests that HF patients have an increased ability to take up or decarboxylate L-DOPA. Sodium restriction resulted in a significant decrease in urinary L-DOPA, DA and DOPAC in HF patients, suggesting that the system responds to sodium. It is concluded that activity of renal dopaminergic system may be altered in SS subjects, despite the level of their BP, and an enhanced delivery of L-DOPA to the kidney may be beneficial in edema formation states.

Reduced Urinary Excretion of Dopamine and Metabolites in Chronic Renal Parenchymal Disease

Background: Chronic renal parenchymal diseases are accompanied by a progressive loss of tubular units endowed with the ability to synthesise dopamine from L-3,4-dihydroxyphenylalanine (L-DOPA), and preliminary evidence has suggested that the urinary excretion of free dopamine may be reduced in these disorders. However, it is well recognised now that under in vitro conditions, dopamine newly synthesised in tubular epithelial cells undergoes extensive deamination to 3,4-dihydroxyphenylacetic acid (DOPAC) by monoamine oxidase (MAO); a small amount of the amine is converted to homovanillic acid by both MAO and catechol-O-methyltransferase (COMT) and a minor amount is methylated to 3-methoxytyramine. Aims: The present study aimed at examining the relationship between renal function and daily urinary levels of L-DOPA, free dopamine and its main metabolites, DOPAC and homovanillic acid (HVA) in patients (n = 28) with chronic renal parenchymal disease, in conditions of controlled sodium, potassium and phosphate intake. The levels of 5-hydroxyindolacetic acid (5-HIAA) were also evaluated in the same cohort of patients. Results: The patients were divided in two groups according to creatinine clearance (group 1, 39±6 ml/min/1.73 m², n = 14; group 2, 139±6 ml/min/1.73 m², n = 14). In patients of group 1, the urinary levels of L-DOPA, dopamine and DOPAC (in nmol/24 h) were significantly lower (60% reduction) than in patients of group 2 (L-DOPA, 134±36 vs. 308±51; dopamine, 759± 175 vs. 1,936± 117; DOPAC 2,595±340 vs. 7,938±833). Also, the urinary excretion of HVA in patients group 1 was significantly lower (40% reduction) than in patients of group 2 (17,434±2,455 vs. 27,179±2,271 nmol/24 h). By contrast, no significant difference was observed in daily urinary excretion of 5-HIAA between the two groups of patients (group 1, 27,280±3,721 nmol/day; group 2, 28,851±2,854 nmol/day). A positive linear relationship was found in these 28 patients between the creatinine clearance and the daily urinary excretion of L-DOPA (r = 0.64, p < 0.001), free dopamine (r = 0.83; p < 0.0001), DOPAC (r = 0.86; p < 0.0001) and HVA (r = 0.65; p < 0.002), but not with that of 5-HIAA (r = 0.14; ns). The U_{dopamine/L-DOPA} and U_{DOPAC/dopamine} ratios were found to be similar in both groups of patients, whereas the U_HVA/DOPAC ratios in patients of group 1 were found greater than in group 2 (p < 0.05). Conclusion: Patients suffering from chronic parenchymal disease with a compromised renal function present with a reduced activity of their renal dopaminergic system which correlates well with the degree of deterioration of renal function. The reduced urinary dopamine output in renal insufficiency is not attributable to enhanced metabolism of renal dopamine. We suggest that the urinary levels of DOPAC may represent a useful parameter for the assessment of renal dopamine synthesis.

Resistant hypertension. Suggestions for dealing with the problem.

With appropriate evaluation of both patient- and physician-related factors, many cases of resistant hypertension can be resolved. Patients often do not understand the implications of their disease and need specific information regarding the importance of compliance with medication schedules and dietary restrictions. Physicians should also consider the possibility of drug resistance or the presence of an identifiable secondary cause, such as renal artery stenosis, chronic renal parenchymal disease, or pheochromocytoma.

Hypertension and renal disease.

Chronic renal parenchymal disease is the most common cause of secondary hypertension: By the time end-stage renal disease develops, its prevalence approaches 75-85%. It was previously believed that hypertension caused arteriolar nephrosclerosis and ischemic renal injury superimposed on primary renal parenchymal disease, contributing to progressive renal insufficiency. Recently, the importance of an increased intraglomerular hydraulic pressure due to loss of renal autoregulation has been emphasized. There are several potential explanations concerning clinical studies which have not uniformly demonstrated slowing of progressive renal damage with antihypertensive therapy: Random BP measurements may not adequately reflect average BP levels, or, alternatively, the widely accepted target level of BP control may be inadequate. In a retrospective study, we found that hypertensive nephropathics had higher serum creatinine levels than normotensives; in another prospective trial we have demonstrated that enalapril is an effective antihypertensive agent in patients with IgA nephropathy, and it also ameliorates the evolution of the disease.

Acquired renal cystic disease in children prior to the start of dialysis.

This report describes the clinical course and serial sonographic findings in three children who developed acquired renal cystic disease (ARCD) prior to the institution of dialysis. The children were aged from 3 years to 13 years and their estimated glomerular filtration rate varied from 8 to 13 ml/min per 1.73 m2 when ARCD was diagnosed. Their primary renal disorders, which included hemolytic-uremic syndrome and focal segmental glomerulosclerosis, had been present for 1.5-11.5 years prior to the cysts being discovered. These patients show that ARCD may develop in children with chronic progressive renal parenchymal disease prior to the institution of specific therapy for end-stage renal disease.

Verapamil Sustained-Release in Renal Parenchymal Hypertension

In 14 patients with arterial hypertension secondary to chronic renal parenchymal disease and impaired renal function, 24-h ambulatory blood pressure, casual blood pressure, plasma concentrations of angiotensin II, aldosterone, arginine vasopressin and atrial natriuretic peptide, serum creatinine, plasma lipids and lipoproteins, and body weight were determined at the end of two consecutive 3-week periods; placebo was administered in the first period and verapamil sustained-release 240 mg was given in the second period. Verapamil reduced mean 24-h ambulatory blood pressure from 152/104 mm Hg (means) to 142/97 mm Hg. Blood pressure was reduced significantly during the daytime, in the evening, and in the early morning, but not at night. Casual blood pressure was also significantly reduced from 176/106 mm Hg to 154/96 mm Hg. No significant changes were determined in the hormones, serum creatinine, plasma lipids and lipoproteins, heart rate, or body weight. Atrial natriuretic peptide was correlated significantly with serum creatinine (p = 0.733, n = 14, p less than 0.01). We conclude that verapamil sustained-release 240 mg in one daily dose has a moderate blood-pressure-lowering effect in patients with chronic renal disease and hypertension without inducing tachycardia, activation of the renin-angiotensin-aldosterone system, or increase in body weight, and without altering renal function and plasma lipids and lipoproteins. The positive correlation between atrial natriuretic peptide and serum creatinine may support the hypothesis that extracellular volume increases during progression of renal disease.

Renal perfusion and function: The implications of converting enzyme inhibition

Abstract Because the kidney is both the source of circulating renin and the final determinant of the state of sodium balance, which in turn defines responsiveness to angiotensin II, one might have anticipated substantial interest in the impact of converting enzyme inhibitors on the kidney when these agents were developed. The lessons learned about the role of the renin-angiotensin system in normal renal perfusion and function, and possible disorders of control that contribute to disease in patients with essential hypertension, renovascular hypertension, and chronic progressive renal parenchymal disease are reviewed. In each case, the lessons here have important implications for the clinical application of converting enzyme inhibition.

Renal perfusion and function: The Implications of Converting Enzyme Inhibition

Because the kidney is both the source of circulating renin and the final determinant of the state of sodium balance, which in turn defines responsiveness to angiotensin II, one might have anticipated substantial interest in the impact of converting enzyme inhibitors on the kidney when these agents were developed. The lessons learned about the role of the renin-angiotensin system in normal renal perfusion and function, and possible disorders of control that contribute to disease in patients with essential hypertension, renovascular hypertension, and chronic progressive renal parenchymal disease are reviewed. In each case, the lessons here have important implications for the clinical application of converting enzyme inhibition.

Sustained release verapamil in renal hypertension.

In 14 patients with arterial hypertension secondary to chronic renal parenchymal disease and impaired renal function, 24-h ambulatory and casual blood pressure readings plasma, angiotensin II, aldosterone, arginine vasopressin and atrial natriuretic peptide, creatinine clearance, plasma lipids and lipoproteins, and body weight were determined after consecutive 3-week periods on placebo and sustained release verapamil 240 mg/day. Verapamil reduced the mean 24-h ambulatory blood pressure from 152/104 to 142/97 mm Hg. Blood pressure was significantly reduced during the daytime and the evening, but not at night. Casual blood pressure was also significantly reduced from 176/106 mm Hg to 154/96 mm Hg. No significant changes were found in the hormones, creatinine clearance, plasma lipids and lipoproteins, heart rate or body weight. The atrial natriuretic peptide level was significantly correlated with the calculated creatinine clearance (r = -0.797). Thus, sustained release verapamil 240 mg as a single daily dose had a moderate hypotensive effect in patients with chronic renal disease without inducing tachycardia, activation of the renin-angiotensin-aldosterone system, or increasing body weight, and without altering renal function and plasma lipids and lipoproteins. The negative correlation between atrial natriuretic peptide and glomerular filtration rate supports the hypothesis that the extracellular volume increases during progression of renal disease.

Hypertensive encephalopathy: Mechanisms, clinical features, and treatment

T HE TERM hypertensive encephalopathy should be reserved for a dramatic clinical syndrome that occasionally punctuates the course of hypertension, either primary or secondary, manifested by subacute alterations in cerebral function that can be reversed by prompt reduction of blood pressure. Unfortunately, this term has been used erroneously to describe a variety of chronic organic brain syndromes occurring in hypertensive patients including residuals of cerebral hemorrhage or cerebral infarction, senile dementia, cortical atrophy, pseudbbulbar palsy, and others. Hypertensive encephalopathy is a medical emergency that demands prompt diagnosis and aggressive treatment before irreversible brain damage or death ensues. From the clinical standpoint, hypertension is the hallmark of hypertensive encephalopathy. Hypertension may be primary (“essential”) or secondary to chronic renal parenchymal disease, renovascular disease, or pheochromocytoma. Hypertensive encephalopathy is rarely observed, if ever, in patients with coarctation of the aorta or primary aldosteronism. The appearance of cerebral symptoms usually follows sudden onset of hypertension or an abrupt increase in blood pressure in patients with already established hypertension. Symptoms appear at lower levels of blood pressure when hypertension is of recent onset rather than when it is chronic. For example, it is not unusual to observe severe headaches, blurred vision, mental obtundation, nausea, vomiting, and focal neurologic signs (including convulsions), characteristic of hypertensive encephalopathy in children with acute glomerulonephritis or women with eclampsia when the blood pressure is no greater than 160/100 mm Hg. However, this syndrome rarely occurs in chronically hypertensive patients until their blood pressure exceeds 2501150 mm Hg.