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Table of Contents
CORRESPONDENCE
Year : 2019  |  Volume : 8  |  Issue : 2  |  Page : 118-119

Authors' response


1 Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
2 Department of Radiodiagnosis, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
3 Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Date of Web Publication11-Nov-2019

Correspondence Address:
K M Bhargav
Assistant Professor, Department of Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517 507, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCSR.JCSR_89_19

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How to cite this article:
Bhargav K M, Kumar B S, Mohan A, Aramadhaka LR, Prajwal B M, Kumar D P, Devi B V, Sivakumar V. Authors' response. J Clin Sci Res 2019;8:118-9

How to cite this URL:
Bhargav K M, Kumar B S, Mohan A, Aramadhaka LR, Prajwal B M, Kumar D P, Devi B V, Sivakumar V. Authors' response. J Clin Sci Res [serial online] 2019 [cited 2019 Dec 16];8:118-9. Available from: http://www.jcsr.co.in/text.asp?2019/8/2/118/270759



We thank Ram[1] for their comments on our paper.[2] As stated in the material and methods section in our paper,[2] we had included the 51 patients that were seen by us, who had consented to participate in the study. When we had conceived the study protocol and had obtained the necessary regulatory approvals, the unified criteria[3] mentioned by Ram[1] were not yet available, and we had defined the diagnosis of autosomal dominant polycystic kidney disease (ADPKD) as per the criteria described by Ravine et al.[4] which were the standard criteria then. In patients with and without family history of ADPKD, the diagnosis was established as per Ravine's criteria.[4] We did not carry out family screening as a part of our study.

The kidney sizes (normal/enlarged/small), presence/absence of chronic kidney disease, anaemia, were documented not as continuous variables and have been presented as such. In ADPKD, reduced renal function with normal-sized kidneys is uncommon. Hence, this was reported.[2]

It is difficult to explain the reason for the cause of reduced kidney size observed in one patient in our study.[2] However, the possibility of chronic infection of the kidneys needs consideration as a possible mechanism. We had noted that renal cell carcinoma was diagnosed in one of the patients. It was an incidental observation and was reported to reiterate the need for generating awareness regarding the malignant potential of ADPKD.

We had documented renal/ureteric calculi on abdominal ultrasonography in 6 (12%) patients. The further detailed evaluation of these patients was beyond the scope of our study protocol. The study protocol was not designed to define the predictors of early hypertension in patients with ADPKD.

We documented headache (n = 11, 21%), altered sensorium (n = 6, 12%) and intracerebral bleed (n = 4) in 11, 6 and 4 patients, respectively. All patients presenting with intracerebral bleed (n = 4; detected on noncontrast computed tomography of the head) had presented with headache and altered sensorium; 2 other patients with altered sensorium and headache had presented with hypertensive urgency; 5 other patients had presented with headache, and in these, hypertension was detected. We have not followed up these patients regarding further detailed neurological work-up as this was beyond the scope of the protocol. As stated earlier, the patient with Marfan syndrome had presented to the medicine outpatient service for the evaluation of breathlessness. Clinical examination confirmed the presence of Marfan syndrome, clinical examination and echocardiography confirmed the diagnosis of mitral valve prolapse in this patient.

As none of our patients were found to have pancreatic, seminal vesicle, ejaculatory and lung cysts and colonic diverticulum, we did not report these details. We agree with Ram[1] that the association between Marfan syndrome and ADPKD has occasionally documented in literature. However, we feel causative role definitely merits further study.

We thank Ram[1] for their observations in [Figure 2]. The image depicted in [Figure 2] is incorrect. The error is regretted. The correct [Figure 2] shows polycystic kidneys on abdominal computed tomography is submitted.
Figure 2: Computed tomography of abdomen showing polycystic kidneys

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ram R. Clinical manifestations, imaging findings and laboratory abnormalities in 51 patients with autosomal dominant polycystic kidney disease: Experience at Tirupati, South India. J Clin Sci Res 2019;8:115-7.  Back to cited text no. 1
  [Full text]  
2.
Bhargav KM, Kumar BS, Mohan A, Aramadhaka LR, Prajwal BM, Kumar DP, et al. Clinical manifestations, imaging fndings and laboratory abnormalities in 51 patients with autosomal dominant polycystic kidney disease: Experience at Tirupati, South India. J Clin Sci Res 2018;7:165-9.  Back to cited text no. 2
  [Full text]  
3.
Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, et al. Unified criteria for ultrasonographic diagnosis of ADPKD. J Am Soc Nephrol 2009;20:205-12.  Back to cited text no. 3
    
4.
Ravine D, Gibson RN, Walker RG, Sheffield LJ, Kincaid-Smith P, Danks DM, et al. Evaluation of ultrasonographic diagnostic criteria for autosomal dominant polycystic kidney disease 1. Lancet 1994;343:824-7.  Back to cited text no. 4
    


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