Hypertension and progression of renal disease

That systemic hypertension is involved in the progression of human renal disease is mostly suggested by the way anti-hypertensive treatment affects the course of the disease. Clinical evidence has been obtained from observational studies as well as from studies of dietary protein restriction. In addition, several trials have compared the effects of different antihypertensive agents. The angiotensin-converting-enzyme inhibitors have the best renoprotective effect when compared to conventional agents and calcium channel blockers. In most studies, ACE-inhibitors approximately halved the risk of progressive renal functional deterioration in patients with non-diabetic nephropathies; this protection was associated with a significant reduction in systemic blood pressure and proteinuria. Statistical analysis, however, also suggests a direct effect of ACE-inhibitors on the kidney.     

Hypertension with elevated renal vein renin secondary to unilateral hydronephrosis

A case of hypertension secondary to unilateral hydronephrosis is reported. Renin levels were elevated in peripheral veins and in the renal vein draining the affected kidney. An infusion of angiotensin II analogue resulted in a decrease in blood pressure. After nephrectomy, blood pressure and peripheral plasma renin activity returned to normal. Renal vein renin and angiotensin II analogue studies were useful in the diagnosis and evaluation of curability by surgery in this case.     

Hypertension and unilateral hydronephrosis

We report 2 cases of hypertension associated with unilateral hydronephrosis. Lateralization of renal vein renins and exaggerated hyperreninemia following captopril suggested renin-mediated hypertension in 1 case, which responded well to nephrectomy.     

Hypertension and unilateral hydronephrosis

Three patients with unilateral hydronephrosis, a normal contralateral kidney, and sustained hypertension were investigated by means of arteriography and differential renal vein renin determinations. The close correlation of the onset of hypertension to the obstructive uropathy, as well as the increased renin production from the affected side, were indicative of a causal relationship. Nephrectomy produced a prompt cure of hypertension in each instance.     

Hypertension in end-stage renal disease patients

The prevalence of hypertension is extremely high in end-stage renal disease, and is a probable contributor to the epidemic of cardiovascular disease in end-stage renal disease. However, the paucity of prospective, randomized clinical trials makes it difficult to precisely define treatment strategies. Therefore, at present time the guidelines developed by the National Kidney Foundation's Cardiovascular Disease Task Force should be followed.     

A case of unilateral renal cystic disease

Unilateral renal cystic disease (URCD) is a distinct entity that is one of the renal cystic diseases. The clinical importance of URCD is to make a differential diagnosis from autosomal dominant polycystic kidney disease (ADPKD), multicystic dysplastic kidney, multilocular cystic renal neoplasm, and simple cysts. To confirm the diagnosis and to rule out asynchronous ADPKD requires long-term follow up, especially in younger patients.     

Hypertension and end-stage renal disease in the developing world

Hypertension is an important primary etiology of end-stage renal disease as well as a major factor responsible for progression of renal disease due to other causes. Multiple genetic and environmental factors are responsible for the variable prevalence of hypertension in various parts of the world. Although the frequency of hypertension awareness and control is very modest in the developing world, nephroangiosclerosis seems to be more common in the developed countries. Factors responsible for this discrepancy as well as various strategic measures to control hypertension and its impact on renal disease are discussed.     

Hypertension and renal injury in experimental polycystic kidney disease

Hypertension and renal injury in experimental polycystic kidney disease. BACKGROUND: Hypertension accelerates renal failure in autosomal dominant polycystic kidney disease (ADPKD), and evidence suggests a role for the renin-angiotensin system (RAS) in the functional and structural changes. To explore the hypothesis that RAS adaptations contribute to disease progression, we examined RAS activity and the long-term consequences of antihypertensive drugs, which suppress (enalapril) or stimulate (hydralazine) the RAS, in experimental polycystic kidney disease. METHODS: Studies were conducted in male heterozygous cystic Han:SPRD rats (Cy/+) and in unaffected littermates (controls). In protocol 1, either angiotensin II (Ang II), enalaprilat, or saline vehicle was acutely infused into cystic and control rats, which were aged 10 to 12 weeks. The mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal plasma flow (RPF) were measured at baseline and after an infusion of test substances. In protocol 2, cystic rats received chronic therapy with either enalapril, hydralazine, or no therapy for 10 to 12 weeks of age and then underwent renal function and RAS studies. In protocol 3, similar cohorts were followed for 40 weeks to assess the effects of therapy on blood pressure, proteinuria, serum creatinine, RAS parameters, and renal morphology. RESULTS: In protocol 1, cystic rats had massive kidneys, slightly elevated blood pressure, and profound renal vasoconstriction and reduced GFR. Ang II induced similar changes in MAP and renal function in control and cystic rats. Enalaprilat induced little effect on MAP but more striking increases in GFR and RPF in cystic rats. In protocol 2, at 10 weeks of age, enalapril was superior in preserving renal function, but neither drug limited the expansion of the tubulointerstitium. In protocol 3, at 40 weeks of age, both drugs ameliorated the increase in serum creatinine, although only enalapril reduced proteinuria and kidney size. CONCLUSIONS: In polycystic rats, acute RAS suppression markedly ameliorates renal dysfunction. However, although chronic enalapril and hydralazine protect against the loss of renal function, only enalapril limits renal growth and proteinuria, and neither significantly limits tubulointerstitial fibrosis. The long-term studies give clear support to the importance of blood pressure control, per se, but only partial support to the importance of the particular agent used. As in clinical studies, angiotensin-converting enzyme inhibition may be less beneficial in ADPKD than in renal diseases characterized by predominant glomerular injury.     

Hypertension associated with unilateral hydronephrosis as a complication of Crohn's disease

Obstructive uropathy with hydronephrosis is a well-known complication of Crohn's disease. The treatment for this condition is still controversial. This is the case study of a 14-year-old girl with documented right-sided obstructive uropathy secondary to Crohn's disease associated with renin-mediated hypertension secondary to her obstructive uropathy. The patient had complete resolution of her hypertension following surgery, which involved only resection of the involved bowel without ureterolysis.     

Synchronous unilateral renal cell carcinoma and Kimura disease of the kidney

Kimura disease (KD) is a rare, benign, chronic inflammatory disorder most often found in young Asian males that can simulate a neoplasm. We report a case of renal cell carcinoma and KD within the same kidney. To our knowledge, this is the first reported case of KD involving the kidney confirmed pathologically, as well as the first association of KD with renal cell carcinoma.     

Kidney growth and renal function in unilateral multicystic dysplastic kidney disease

The natural history of multicystic dysplastic kidney (MCDK) is not well established. We analyzed kidney growth and renal function in 33 children with prenatally diagnosed unilateral MCDK in a long-term study. The mean observation period was 4.9 years with a range of 1–11.6 years. Abnormalities of the contralateral kidney were found in 10 of 33 patients (30%): ureteropelvic junction obstruction (5), ureterovesical junction obstruction (2), and vesicoureteral reflux (3). In 6 children the dysplastic kidney had been removed. Complete involution was observed in 48% and a decrease of size in 33% of 27 dysplastic kidneys. At the time of last examination, 27 of 29 children showed a volume of the contralateral kidney above the normal range (>145%). Hypertrophy of the contralateral kidney, defined as kidney length above 2 standard deviation scores (SDS), was seen in 24% of 33 children at birth, thus showing that hypertrophy of the contralateral kidney starts in utero and continues throughout childhood. The extent of contralateral hypertrophy was independent of associated abnormalities in this study. Mean creatinine was increased in the whole group (mean +1.13 SDS). Calculated creatinine clearance in 21 patients over 2 years was within normal limits, with a median of 102 ml/min per 1.73 m² (range 84–143). Based on the results of this and previous studies, nephrectomy cannot be recommended in typical cases, but a regular follow-up of these patients seems necessary. Received September 18, 1997; received in revised form February 17, 1998; accepted February 18, 1998     

Total unilateral renal destruction caused by irradiation for Hodgkin's disease

Total unilateral renal destruction has been observed in a patient who previously received irradiation for Hodgkin's disease. The clinical features, after a six-year asymptomatic interval, included recurrent calculi and infection in what was subsequently demonstrated radiographically to be a nonfunctioning kidney. The gross and microscopic characteristics of the nephrectomy specimen have been described and correlated with the magnitude of irradiation and the clinical course.