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PubMed1980

[Increase of renal failure after treatment of malignant hypertension by captopril (author's transl)].

In a 25-year-old woman with malignant hypertension based on primary nephrosclerosis, captopril, an oral inhibitor of angiotension I-converting enzyme, lowered blood pressure effectively, which had been resistant previously to other oral antihypertensive drugs. Concomitantly with the decrease of the high blood pressure, an increase of creatinine from 2.1 mg% to 8.5 mg% occurred. There is evidence that this increase of renal failure is a consequence of blood pressure reduction and is not caused by a toxic effect of captopril.

Adult↗

PubMed2003

[Ultrasound of the kidney and renal vessels. I: Normal findings, congenital diseases, diseases of the kidney parenchyma].

Renal ultrasonography has become the standard imaging modality in the investigation of kidneys because it displays excellent anatomic detail, requires no special preparation of the patient and does not expose the patient to radiation or contrast agents. Ultrasonography is used to determine the site and size of the kidney and to detect focal lesions like tumors, cysts and renal stones. Furthermore the presence and urodynamic relevance of hydronephrosis can reliably be revealed. Also renoparenchymatous diseases are discernible to the experienced investigator, however most glomerular diseases cannot be further subclassified. Exceptions are primarily renovascular disorders like hypertensive nephrosclerosis, diabetic nephropathy or renal vasculitis. Color Doppler sonography allows the detection and quantification of renal artery stenosis, increased resistance index values may indicate irreversible disease. Ultrasonography has also been found of value in the evaluation of renal transplant kidneys. Especially in the early transplant course potentially fatal but reversible diseases like renal vein thrombosis or urinomas are detected with high sensitivity. In the long term, an increased resistance index value may also predict allograft failure.

Blood Flow Velocity↗

PubMed2005

[Ultrasonography of the kidney and renal vessels. I. Normal findings, inherited and parenchymal diseases].

Renal ultrasonography has become the standard imaging modality in the investigation of kidneys because it displays excellent anatomic detail, requires no special preparation of the patient and does not expose the patient to radiation or contrast agents. Ultrasonography is used to determine the site and size of the kidney and to detect local lesions like tumors, cysts and renal stones. Furthermore the presence and urodynamic relevance of hydronephrosis can reliably be revealed. Also reno-parenchymatous diseases are discernible to the experienced investigator, however most glomerular diseases cannot be further subclassified. Exceptions are primarily renovascular disorders like hypertensive nephrosclerosis, diabetic nephropathy or renal vasculitis. Color Doppler sonography allows the detection and quantification of renal artery stenosis, increased resistance index values may indicate irreversible disease. Ultrasonography has also been found of value in the evaluation of renal transplant kidneys. Especially in the early transplant course potentially fatal but reversible diseases like renal vein thrombosis or urinomas are detected with high sensitivity. In the long term, an increased resistance index value may also predict allograft failure.

Humans↗

PubMed2005

Pulmonary resection for non-small-cell lung cancer in patients on hemodialysis: clinical outcome and long-term results.

Patients on hemodialysis (HD) who undergo surgery represent a high risk group requiring careful perioperative management to avoid electrolyte imbalance and hemodynamic instability. The aim of the study was to analyze the postoperative outcome in terms of complications and survival of a group of patients on HD who had undergone pulmonary resection for non-small cell lung cancer (NSCLC). Six patients on HD underwent seven pulmonary resections at our institution from 1998 to 2003. The underlying kidney disease was nephrosclerosis in two patients and glomerulonephritis in four. The mean levels of blood urea nitrogen and serum creatinine were 107 +/- 11.5 mg/dl and 7.9 +/- 0.64 mg/dl, respectively. The mean preoperative PO2 and FEV1 were 77.6 +/- 2.4 mmHg and 2.4 +/- 0.16 liters, respectively. The histologic diagnosis was squamous cell carcinoma in four cases and adenocarcinoma in three. One patient underwent two lung resections in 4 years for two primary lung cancers. Five patients underwent lobectomy, one underwent a wedge resection, and in one case pneumonectomy was performed after neoadjuvant chemotherapy. There was no operative mortality. Postoperatively, atrial fibrillation occurred in two patients associated with sputum retention in both, and two other patients had hyperkalemia (complication rate 57%). One patient died of cardiac complications 27 months after surgery. The remaining five patients are currently alive with no evidence of disease. Patients on HD who undergo lung resection have a high rate of postoperative complications. Although the underlying disease influences long-term survival, radical lung resection in NSCLC patients is recommended in selected cases. Careful metabolic, hematologic, and pharmaceutical management is mandatory during the perioperative period.

Adenocarcinoma↗

PubMed1998

The Tsukuba hypertensive mouse (transgenic mouse carrying human genes for both renin and angiotensinogen) as a model of human malignant hypertension: development of lesions and morphometric analysis.

The renin-angiotensin system has a pivotal role in hypertension. The Tsukuba hypertensive mouse (THM; a transgenic mouse carrying human genes for both renin and angiotensinogen) was generated to allow further examination of the renin-angiotensin system in a variety of pathologic conditions. We evaluated the development of renal lesions in these mice and in controls by morphometric, immunohistochemical and ultrastructural methods. Blood pressure was significantly higher in THM than in control mice; 1 year after birth, it was approximately 40 mmHg higher. The kidney-to-body weight ratio was also higher in THM than in control. Morphometrical analysis revealed that the glomerular sclerosis index was significantly elevated in THM with 10% of the glomeruli sclerotic at 18 months. The grade of vascular lesion and the frequency of fibronoid arteritis of the kidney exhibited the same tendency as the glomerular sclerosis index. Murine renin was located exclusively in the juxtaglomerular apparatus, whereas human renin was expressed not only in the juxtaglomerular apparatus, but also in periarteriolar smooth muscle cells and in mesangial and epithelial cells of the glomeruli. Light and electron microscopy revealed significant fibrinoid arteritis of the kidney in THM and also "onion skinning", both pathognomonic for malignant nephrosclerosis. THM may be an excellent model of human malignant hypertension.

Animals↗

PubMed2004

Generalized atherosclerosis sparing the transplanted kidney in Schimke disease.

Schimke-immuno-osseous dysplasia (SIOD) is a multisystem disorder caused by a mutation of the chromatin remodeling protein. The main clinical findings are spondyloepiphyseal dysplasia with disproportional growth deficiency, nephrotic syndrome with focal and segmental glomerulosclerosis, and defective cellular immunity. Transitory ischemic attacks due to vaso-occlusive processes are still an untreatable and life-limiting complication in patients with SIOD. The underlying pathophysiology of vaso-occlusive processes in SIOD is unclear. We report the clinical and pathological findings of the eldest published patient with the severe form of SIOD, who died at the age of 23 years due to pulmonary hypertension with subsequent right heart failure. The autopsy revealed a severe generalized atherosclerosis including the brain, heart, and pulmonary arteries. However, the kidney that was transplanted at the age of 5 years showed a good graft function without glomerular sclerosis and with only minimal nephrosclerosis on histology. Thus, the absence of severe vaso-occlusive processes in the transplanted organ and in the severely atherosclerotic host may indicate that the vaso-occlusive processes in SIOD are not caused by post-transplant cardiovascular morbidity such as arterial hypertension and hyperlipidemia. Instead, vascular factors of the host such as endothelial dysfunction may explain the pathophysiology of atherosclerosis in SIOD.

Adolescent↗

PubMed2001

Low birth weight-associated adult hypertension in the rat.

Epidemiological surveys have suggested that intrauterine growth retardation is a risk factor for the development of hypertension in later life. A rat model of intrauterine growth retardation, induced by maternal low-protein diet during the second half of pregnancy, was used to study the relationship between birth weight and adult hypertension. The offspring were born at term and were allowed to nurse normally until weaned to standard chow at 4 weeks of age. They had 15% lower birth weights than control offspring, with complete catch-up growth by age 4 weeks. Both females and males developed progressively worsening hypertension beginning at 8 weeks. The 11-month survival rate was 69% versus 100% in control animals. During the early stages of the hypertension, plasma creatinine was normal, plasma sodium concentration was slightly higher than that of control animals, plasma renin activity was suppressed, and the males had mild proteinuria. Renal function remained normal throughout the 11-month observation period, but plasma renin activity gradually rose above control values. Angiotensin-converting enzyme inhibition by enalapril, begun at 8 weeks of age, was effective in completely normalizing the blood pressure, but did not totally prevent the extra mortality. Sprague-Dawley and Wistar rat strains developed equally severe hypertension after maternal protein deprivation, despite their different susceptibilities to nephrosclerosis with aging. In conclusion, maternal low-protein diet resulted in low birth weight and adult hypertension in the rat. Primary sodium retention and expanded extracellular volume may be critical factors during the development of the hypertension.

Animals↗

PubMed2006

Polyamines in renal failure.

The levels of polyamines (putrescine, spermidine and spermine) and polyamine oxidase in plasma of patients with chronic renal failure were determined. The level of putrescine was increased but the level of spermine was decreased in the plasma of these patients. The patients also had increased plasma polyamine oxidase activity leading to increased degradation of spermine. As acrolein was a major toxic compound produced from spermine by polyamine oxidase, the levels of free and protein-conjugated acrolein in plasma were also measured. Acrolein levels were enhanced in plasma of patients with chronic renal failure. The accumulated acrolein found as protein conjugates was equivalent to 170 microM, which was about 5-fold higher than in plasma of normal subjects. It was found that acrolein is mainly produced by spermine oxidase in plasma. An increase in putrescine, spermine oxidase and acrolein in plasma was observed in all cases such as diabetic nephropathy, chronic glomerulonephritis and nephrosclerosis. After patients with chronic renal failure had undergone hemodialysis, their levels of plasma polyamines, spermine oxidase and acrolein returned towards normal. It is likely that acrolein produced from spermine accumulates in the blood due to decreased excretion into urine and may function as a uremic "toxin".

Acrolein↗

PubMed2005

Tuberous sclerosis, associated with renal cell carcinoma and angiomyolipoma, in a patient who developed endstage renal failure after nephrectomy.

We report a case of tuberous sclerosis (TSC) associated with renal cell carcinoma and angiomyolipoma in a patient, who developed endstage renal failure that required hemodialysis after nephrectomy. A 37-year-old woman with TSC was admitted for further investigation of bilateral renal masses detected by computed tomography (CT). Angiography revealed a tumor stain (4 cm in diameter) in the medial portion of the right kidney. Because renal cell carcinoma (RCC) was strongly suspected, right nephrectomy was performed. Her serum creatinine level was already increased, moderately, at 2.4 mg/dl, before the right nephrectomy. Her renal function deteriorated quickly (in 1(1/2) years) after the right nephrectomy, and hemodialysis was introduced the next year. The histological findings of the resected right kidney revealed marked intimal thickening of the intralobular arteries. These findings suggested that the renal function loss was not only caused by the nephron mass reduction due to the nephrectomy but was also caused by nephrosclerosis. Though most patients with TSC die before developing endstage renal failure, this patient is currently receiving maintenance hemodialysis and has been followed for 3 years with no recurrence of RCC in the left kidney.

Adult↗

PubMed2006

Care of elderly patients with chronic kidney disease.

BACKGROUND: Providing optimal care to the growing number of chronic kidney disease (CKD) patients remains a significant problem in the United States. There is little known about the care of elderly CKD patients by primary care physicians as well as nephrologists. METHODS: We performed a retrospective study of 377 elderly male CKD (serum creatinine >1.4 mg/dl on 2 separate occasions 3 months apart) patients referred to the Nephrology Clinic at the Buffalo Veterans Administration Medical Center between 1999 and 2002 to see if the pattern of care changed during this time. RESULTS: The mean age of the patients was 75.9 years. Eighty-four percent were Caucasian, 15% were African-American, and 1% were of other race. Etiology of CKD included hypertensive nephrosclerosis (49%), diabetic nephropathy (23%), renovascular disease (18%), and others (10%). Sixty-five percent of patients had estimated glomerular filtration rate (eGFR) >30 ml/min. Overall angiotensin converting enzyme inhibitor (ACEI) was used in 51% of patients with CKD, and in 63% of patients with diabetic nephropathy. Twenty percent of patients had a hemoglobin <11 g/dl, darbepoietin/epogen was used in 31% of these patients. Screening for kidney related tests were done infrequently while lipid profile and hemoglobin A1C were done in the majority of patients because of clinical reminders in the VA computerized patient record system (CPRS). CONCLUSION: These results emphasize the need for increased education of primary care physicians and nephrologists to improve the care of elderly CKD patients. Although there was a trend towards earlier referral, care did not change significantly between years 1999 and 2002.

Aged↗

PubMed2006

Clinical spectrum of chronic renal failure in the elderly: a hospital based study from eastern India.

The aim of this study was to describe the clinical spectrum of chronic renal failure (CRF) in the elderly. The diagnosis of CRF was made using standard clinical criteria. The elderly was defined as person with over 60 years of age. In total, 200 elderly patients with CRF were evaluated between July 2002 and February 2004. Their age (male: 146; female: 54) ranged between 60 and 90 (mean 64.31+/-4.18) years. Diabetic nephropathy was the most common (46%) cause of CRF. Hypertensive nephrosclerosis, chronic interstitial nephritis and obstructive uropathy were responsible for CRF in 18%, 14% and 13% of patients, respectively. We observed chronic glomerulonephritis in 7% of elderly CRF. Urinary tract infection (55.5%), hypovolemia (22.2%), accelerated hypertension (11.1%) and sepsis (11.1%) were responsible for acute exacerbation of renal failure in 36 (18%) patients. Associated co-morbid conditions were noted in 93 (46.5%) patients. They included; coronary artery disease 46 (49.46%), cerebrovascular disease 20 (21.50%), osteoarthritis 13 (13.97%), chronic obstructive pulmonary disease 6 (6.45%), dilated cardiomyopathy 5 (5.37%), and malignancy in 3 (3.22%) patients. Acute dialytic support was required in 164 (82%) cases and remaining 36 (18%) patients received conservative management. Mortality was noted in 25 (12.5%) cases. The coronary artery disease (48%), acute pulmonary edema (20%) and hyperkalemia (12%) were the main causes of death. Subsequent evaluation revealed that 102 (51%) patients had ESRD of which only 3 (2.94%) patients could afford CAPD. A total of 11 (10.7%) patients underwent chronic maintenance hemodialysis for 3-4 months and then discontinue dialysis mainly because of financial constraints. Remaining 88 (86.27 %) patients with ESRD were discharged from hospital after symptomatic improvement with acute dialysis. Thus, diabetic nephropathy related to type-2 diabetes was the commonest cause of CRF in our elderly patients. Chronic renal failure in elderly was associated with a number of co-morbid conditions, which contributed significantly to morbidity and mortality. Acute on chronic renal failure with severe uremic complications were an important cause of hospitalization. The financial constraint was the major limiting factor for the management of elderly ESRD patients.

Aged↗

PubMed2006

Uric acid: its relationship to renal hemodynamics and the renal renin-angiotensin system.

Reports relating hyperuricemia and hypertension have been filed for many decades. Nevertheless, controversy remains concerning serum uric acid concentration as an independent risk factor underlying coronary heart disease (CHD) and essential hypertension or as an indirect marker of renovascular involvement. Earlier studies in normotensive subjects and hypertensive patients demonstrated that serum uric acid concentration was closely related to intrarenal hemodynamic alterations, suggesting that it is an excellent marker of vascular involvement. Our data from clinical studies and in an animal model of severe hypertensive nephrosclerosis have strengthened this concept. Conversely, other reports have suggested that uric acid may be a pathogenetic factor. Supporting arguments for this theory maintain that experimental hyperuricemia induces hypertension and renal damage. Epidemiologically, hyperuricemia is associated with hypertension, CHD, renal disease, toxemia of pregnancy, and other outcomes, although mechanisms remain unclear. Additionally, there are no available data on the effects of lowering uric acid on pressure control and organ protection.

Humans↗

PubMed2006

Development of microalbuminuria in essential hypertension.

During the past few years, microalbuminuria has become a prognostic marker for cardiovascular and/or renal risk in diabetic and nondiabetic subjects. In essential hypertensives, an increased transglomerular passage of albumin may result from several mechanisms--hyperfiltration, glomerular basal membrane abnormalities, endothelial dysfunction, and nephrosclerosis. Cross-sectional studies have demonstrated that the main factors related to microalbuminuria are blood pressure (BP) values and hyperinsulinemia, as an expression of insulin resistance. Genetics, obesity, and smoking, however, have also been implicated as determinants of microalbuminuria in some of the studies. Follow-up studies support the role of BP values and subtle alterations in glucose metabolism, although contributing roles need to be assessed in further studies. It seems that the significance of microalbuminuria in essential hypertension is much broader than expected, and several factors may influence the presence of microalbuminuria. Thus, to reverse microalbuminuria, and to reduce urine albumin excretion and cardiovascular and renal risk, a strategy of multiple approaches may be needed. Whether or not the multiple approaches need to be implemented from the beginning or step by step in an individual approach should be established in the near future.

Albuminuria↗

PubMedDate not supplied

The kidney as a target of hypertension.

In spite of improvement in blood pressure control during the last decades, the incidence of hypertension-related end-stage renal disease (ESRD) is reported to have increased and has become a common cause of renal failure, especially in the United States, but also in several other countries. The clinical diagnosis of hypertensive nephrosclerosis is usually presumptive, and an important differential diagnosis in older hypertensive persons is atheromatous renal vascular disease. Many studies of renal function in treated essential hypertension have shown a small and clinically insignificant decline in glomerular filtration rate (GFR). Recent long-term studies indicate that the change in GFR may be nonlinear, with a greater fall in GFR after initiation of antihypertensive treatment, followed by a phase of minimal or normal loss of GFR. There are no available prospective studies indicating that well-treated essential hypertension leads to renal failure, but there are new data indicating that patients with nonmalignant essential hypertension without any underlying renal disease and with early and good blood pressure control do not develop renal failure.

Glomerular Filtration Rate↗

PubMed1987

Systemic hypertension and the kidney in black patients.

Hypertension occurs more frequently in U.S. blacks than whites and is more severe. Blacks represent a disproportionate percentage of patients receiving dialysis treatment. This disproportion raises the question of whether the renal circulation of blacks is more sensitive to the damaging effects of elevated intraarterial pressure or whether it is structurally different in ways that would render it more prone to damage. The first part of the question has not been conclusively answered although some data support the hypothesis. For the second part, it is clear that malignant nephrosclerosis of blacks is different from that of whites in an absence of fibrinoid necrosis of arterioles and glomeruli and the presence of musculomucoid intimal hyperplasia of small arteries. Whether this is a genetically determined reaction to damage has not been determined. It is a widely held belief that the kidney is the cause of much essential hypertension. In fact 6 cases of essential hypertension in blacks have been "cured" by renal transplantation, strongly supporting the belief. Also blacks differ from whites in 2 ways that could be relevant for their increased prevalence of hypertension: they excrete sodium loads more slowly and have a markedly lower urinary kallikrein. The former could be responsible for the predominance of salt-dependent hypertension in blacks and the latter could reflect a racial deficiency in a naturally occurring vasodilator system.

Adolescent↗

PubMed1982

Diuretic potency of combined hydrochlorothiazide and furosemide therapy in patients with azotemia.

The effect of combined hydrochlorothiazide and furosemide therapy was studied in eight hypertensive patients with renal insufficiency who had poor response to either furosemide or hydrochlorothiazide alone. The study was divided into two parts. In part A, five patients had an inadequate response to furosemide in doses of 160 to 240 mg/day followed a strict protocol in order to compare the effect of increased doses of furosemide with combined hydrochlorothiazide-furosemide administration. All had azotemia, presumable from nephrosclerosis, and had serum creatinine concentrations ranging from 2.3 to 4.9 mg/dl. Four of the five patients had inadequate arterial pressure control, and the remaining patients had fluid retention from the administration of minoxidil. In all five patients, plasma volume was either increased or normal, despite long-term treatment with furosemide. Increasing the dose of furosemide to between 320 and 480 mg/day had only a modest additional diuretic effect, and plasma volume and arterial pressure were not significantly changed. Adding hydrochlorothiazide, 25 to 50 mg twice a day, produced a marked diuresis, and a significant reduction in weight, plasma volume and mean arterial pressure (p less than 0.025 for all three patients). In part B, combined hydrochlorothiazide-furosemide therapy was used to treat three additional patients who had an inadequate response to either diuretic alone. The results indicate that combined hydrochlorothiazide-furosemide is a potent diuretic regimen and is effective in many patients wit chronic renal failure who have a poor response to furosemide alone.

Adult↗

PubMed1984

Obesity in hypertension: how innocent a bystander?

Hypertension and obesity frequently coexist in the same patient. However, the two disorders disparately affect cardiovascular function and structure. The presence of obesity significantly affects hypertensive target organ involvement. On one hand, obesity may tend to mitigate the harmful effects of a chronically elevated total peripheral and renal vascular resistance and lessen end-organ damage such as nephrosclerosis in essential hypertension. However, since both obesity and hypertension increase cardiac workload, although by different mechanisms, their presence in the same patient results in a double burden to the left ventricle. Congestive heart failure, sudden death, and coronary heart disease are common sequelae of obesity hypertension. Weight loss reduces arterial pressure by a decrease in intravascular volume and cardiac output associated with a fall in sympathetic activity. Intervention in obesity hypertension diminishes the dual hemodynamic burden imposed on the heart and becomes therefore a major objective in the prevention and treatment of heart disease.

Adaptation, Physiological↗

PubMed1992

Hypertensive nephropathy: is a more physiologic approach to blood pressure control an important concern for the preservation of renal function?

During the past 2 decades, there have been important reductions in stroke-related morbidity and mortality due to better control of hypertension. However, there has been a lesser effect on the reduction of coronary mortality and far less of an impact on all other forms of noncardiovascular disorders such as renal disease. This suggests that our ability to prevent hypertensive nephrosclerosis through traditional methods of lowering blood pressure may not be as effective as was once thought, particularly in high-risk patients such as blacks, diabetics, the elderly, and patients with preexisting renal disease. One reason that may partially explain the difficulty in protecting the renal circulation from hypertensive damage is the interaction between antihypertensive medications and the aged-related decline in renal perfusion. Depending on their mechanism of action, antihypertensive agents may impair renal blood flow (through plasma volume contraction or reduction) and further aggravate the age-related decline in renal perfusion. A worsening of renal perfusion may activate counterregulatory neurohormonal mechanisms, such as the renin-angiotensin-aldosterone system, which in turn may place the patient at increased risk for the development of glomerulosclerosis through promotion of vascular or mesangial hypertrophic changes or increased intraglomerular pressure, despite an associated reduction in systemic blood pressure. Since antihypertensive agents have such varied effects on systemic and renal hemodynamics, an understanding of the antihypertensive actions in a given patient may have significant influence on renal function. Thus, an improved understanding about the effects of aging and hypertension on the renal microcirculation will hopefully facilitate a more physiologically appropriate antihypertensive medication selection with the expectation that renal function will be benefitted over the long term.

Age Factors↗